Convulsive syndrome, paroxysmal disorders of consciousness. Paroxysmal disorders of consciousness, fainting

Purpose: To study non-epileptic paroxysmal disorders of consciousness

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20. NEUROTIC ATTACKS (AFFECTIVE-RESPIRATORY AND PSYCHOGENIC ATTACKS, PANIC ATTACKS)

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22. NONEPILEPTIC PAROXYSMS DURING SLEEP

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27. EXTRAPYRAMIDAL DISORDERS (TICS, TOURETTE’S SYNDROME, PAROXYSMAL C0PE0ATET03, NONEPILEPTIC MYOCLONUS)

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There are many diseases whose symptoms can have a significant negative impact on health. In addition to this fact, there is also such a problem as a paroxysmal state of the brain. Its essence boils down to the fact that the symptoms of certain diseases significantly increase for a short period of time. Such a process can pose a serious threat to human life, which is why it definitely deserves attention.

Paroxysmal syndrome

In order to understand the essence of this diagnosis, you need to understand some terms. By paroxysm, or attack, we mean a transient dysfunction of any system or organ that occurs suddenly. This condition is divided into two main types: epileptic and non-epileptic.

But speaking generally, we are talking about a situation where a certain painful attack sharply intensifies to the highest degree. In some cases, the term “paroxysmal state” is used to describe recurrent symptoms of a specific disease. We are talking about health problems such as swamp fever, gout, etc.

In fact, paroxysms are a reflection of emerging dysfunction of the autonomic nervous system. The most common causes of such attacks are neuroses, hypothalamic disorders and organic brain damage. Crises may be accompanied by migraines and attacks of temporal lobe epilepsy, as well as severe allergies.

Despite the fact that there are several forms through which the paroxysmal state manifests itself, symptoms with similar characteristics can be found in all cases. We are talking about the following signs: stereotypicality and tendency to regular relapses, reversibility of disorders and short duration. Regardless of the background of what disease the paroxysm made itself felt, these symptoms will be present in any case.

Provoking factors

So, understanding that the basis of such a problem as a paroxysmal state is in fact always cerebral disorders, it is worth paying attention to those diseases that can lead to a sudden deterioration in physical condition, without the appearance of noticeable symptoms before.

It is this fact that allows us to assert that with all the abundance of various pathologies that serve as the background for a crisis, it is almost always possible to trace a single etiological picture.

You need to understand that doctors pay enough attention to this problem, so a study was carried out on the condition of a significant number of patients in order to identify common etiological factors that lead to the occurrence of paroxysms. The examinations were focused primarily on working with diseases such as vegetative-vascular dystonia, migraine, epilepsy, neuralgia and neuroses, etc.

What diseases lead to a crisis?

As a result of the above-mentioned studies, a list of diseases that have characteristic signs of paroxysm was compiled:

Metabolic disorders and diseases of the endocrine system. These are climacteric Cushing's, pheochromocytoma, hypercapnia and hypoxia.

Alcohol and drug poisoning can also provoke paroxysmal conditions. Technical poisoning and certain types of medications can have a similar effect.

A sharp increase in symptoms is possible with diseases of internal organs such as pneumonia, hepatic coma, etc.

Paroxysm can also manifest itself against the background of illnesses (neuroses, migraines, hysteria, depressive states, etc.).

Hereditary diseases also play an important role in provoking such a problem as a paroxysmal state. This may be the impact of metabolic diseases, systemic degenerations of the central nervous system, etc.

Don't discount the type. We are talking primarily about post-traumatic cerebrovascular disease, traumatic brain injury and causalgia. But vascular pathologies of the brain, as well as neuralgia and ischemic diseases, can also play a negative role.

How paroxysm can manifest itself: features

As mentioned above, in the vast majority of cases, a sharp exacerbation of symptoms occurs due to dysfunction of the brain. In addition, manifestations that are directly related to cerebral disorders are often recorded, and this is one of the key features of this condition.

In addition, you need to understand that there are both primary and secondary paroxysmal genesis. Primary is caused exclusively by congenital factors of manifestation, such as disorders in the brain and genetic disposition, which is formed during the development of the embryo. Secondary paroxysm is a consequence of the influence of internal and external factors. It manifests itself already during life.

The peculiarities of such a problem do not end there. Such paroxysmal states are recorded in neurology, which accompany the disease throughout the entire period of its course. Also, a sharp increase in symptoms may be one-time in nature and result from a state of shock in the central nervous system. One striking example is acute blood loss or a sudden increase in temperature.

There are also cases when paroxysmal attacks, being short-term and regular, affect the condition of the whole organism. Such attacks often occur against the background of migraine.

Such changes in the body can perform a protective function, due to which the compensatory component is stimulated. But this is possible only at an early stage of the disease. But the syndrome of paroxysmal states is very dangerous, since it turns into a significant complicating factor in diseases that initially cannot be called simple.

Results of examination of children's condition

In order to understand what non-epileptic paroxysmal states look like in children, it makes sense to pay attention to several current examples.

First of all, these are short-term breath holdings. This problem can be caused by severe fear, frustration, pain, or any surprise. During this condition, the child may scream, while the scream itself is delayed while exhaling, which is often followed by loss of consciousness. Sometimes clonic twitching appears. Such an attack usually lasts a minute. Severe bradycardia and voluntary urination are possible.

Attacks of this kind are most often recorded in the age period from 6 months to 3 years. The good news is that their presence does not increase the risk of cognitive decline or epilepsy.

Paroxysmal state in a child - what is it? It is worth paying attention to one more example that clearly demonstrates a similar problem. We are talking about Fainting in this case is the result of acute circulatory failure in the brain area. In fact, this is nothing more than a manifestation of vascular lability.

Fainting occurs mainly in adolescents; among children who are at an early age, such conditions are rare. As for the causes of this problem, they include a sharp transition from a horizontal to a vertical position, as well as a state of strong emotional arousal.

Fainting begins with a feeling of darkening in the eyes and dizziness. In this case, both loss of consciousness and loss of muscle tone occur at the same time. There is always a possibility that short-term clonic convulsions may occur during depression of the child’s consciousness. As a rule, children do not remain unconscious due to fainting for more than 1 minute.

Reflex epilepsy is another problem that can be caused by a paroxysmal state in a child. It is unnecessary to say that this is a rather dangerous condition. Stressful situations and flashes of light can provoke such manifestations. But complex activities and auditory stimuli are unlikely to cause reflex epilepsy.

Non-epileptic form

When considering the syndrome of paroxysmal states, it is worth paying attention to those diseases that most often accompany such crises.

We can distinguish four main types of diseases within this group, which are recorded in the clinic more often than others and, in turn, have other, more specific forms. We are talking about the following problems:

Headache;

Myoclonic syndromes and other hyperkinetic states;

Autonomic disorders;

Muscle dystonic syndromes and dystonia.

In most cases, these problems are recorded in patients who have not reached the age of majority. But recently, more and more often, the paroxysmal state makes itself felt for the first time already in adulthood. It is also possible for the symptoms of the above diseases to dynamically progress, which become more severe against the background of chronic or age-related cerebral disorders.

It is also important to take into account the fact that in some cases, non-epileptic paroxysmal conditions may be a consequence of the effects of certain medications prescribed to neutralize circulatory failure, as well as diseases such as parkinsonism and some mental disorders caused by old age.

Epilepsy and paroxysmal conditions

This is a rather difficult diagnosis in terms of the level of its negative impact on a person. But first, it is worth remembering that we are talking about a chronic pathological disease of the brain, which is characterized by seizures that have a different clinical structure and are constantly recurring. This condition is also characterized by psychopathic paroxysmal and non-convulsive manifestations.

It is possible to develop two forms of epilepsy: genuine and symptomatic. The latter is a consequence of traumatic brain injury, intoxication, brain tumors, acute circulatory disorders in the head, etc.

It is worth understanding that the special relationship between the epileptic focus and different parts of the nervous system determines the occurrence of repeated seizures of various clinical structures. Some features of the pathological process can lead to this result.

In addition, other paroxysmal conditions may occur

Different forms of seizures

Epilepsy is not the only form of manifestation of disorders of the central nervous system. There are other paroxysmal conditions in neurology that can be classified as epileptic.

One of the striking examples is sensory (sensitive). Their manifestation occurs when a person is conscious. Symptoms include tingling and numbness in the face, limbs and half of the torso. In some cases, sensory seizures can turn into motor ones, which will significantly complicate the patient’s condition.

Attention should also be paid to Jacksonian epilepsy. In this case, both sensory and motor seizures are possible. The latter are especially problematic because they involve muscle spasms in the part of the face and limbs that are located on the side opposite the epileptic focus. In this case, disturbances in consciousness, as a rule, are not observed. In some cases, motor seizures can become generalized.

Complex absence seizures can be atonic, myoclonic, or akinetic. The first make themselves known through a sudden fall, the cause of which is a sharp decrease in the postural tone of the legs. As for the myoclonic form, it is characterized by short-term rhythmic movements accompanied by a loss of consciousness. Akinetic absence seizure is a seizure with immobility, which can also result in falls.

Small absence seizures are also possible, in which a person also plunges into an unconscious state. There are no feelings of discomfort after its completion. The patient often cannot remember the moment of the attack.

It is characterized by limited short convulsions that are clonic in nature. They most often capture the muscles of the arms, but the tongue, face and even legs can be affected by this process. Loss of consciousness during such convulsions is a rare occurrence.

Generalized status epilepticus

This form of seizures is serious enough to warrant special attention. In fact, we are talking about the development of tonic-clonic seizures in all parts of the body. This paroxysmal state appears suddenly, with mild muscle tension and moderate dilation of the pupils. The symptoms do not end there and go into the tonic phase, lasting from 15 minutes to half an hour.

The tonic phase is characterized by tension in the torso, limbs, as well as masticatory and facial muscles. In this case, the body tone becomes so high that it is virtually impossible to change the position of the body.

As for the clonic phase, its duration is 10-40 s, during which rhythmic closure of the oral fissure is recorded. In this condition, there is a high risk that the person will bite the tongue, which may result in reddish foam (stained with blood) coming out of the mouth.

The next phase of the generalized status is relaxation, which is expressed in spontaneous defecation and urination. The troubles do not end there: each attack ends with post-paroxysmal exhaustion. In other words, depression of reflexes, muscle hypotonia and deepening of coma occurs. This state lasts on average 30 minutes. Next comes the final phase of epileptic prostration.

How to help with seizures

Treatment of paroxysmal conditions - This is the lot of highly qualified specialists. Therefore, if signs of a single seizure become noticeable, especially when it is the first, the patient must be urgently hospitalized in a neurosurgical or neurological department. There they will be able to examine him and determine the current treatment plan.

It is important to ensure that the patient does not suffer any injuries before being taken to the hospital. It is also worth putting a spoon wrapped in a bandage into the mouth or using a mouth dilator.

In most cases, the treatment process for patients with status epilepticus begins in the ambulance. If doctors are not yet around, and the person is still having a seizure, then the first thing to do is to rule out the possibility of aspiration of vomit or mechanical asphyxia due to tongue prolapse. To do this, you need to insert the air duct into your mouth, first releasing it. It also makes sense to try to block seizures and maintain cardiac activity.

As for non-epileptic forms, the causes of paroxysmal states can be completely different. It all depends on the key disease, the symptoms of which are aggravated. Therefore, the best thing that can be done is to take the person to the hospital as quickly as possible, where he can be examined and an accurate diagnosis made.

Results

Paroxysmal conditions can be classified as a category of diseases that can not only significantly worsen a person’s condition, but also lead to death. This means that if you experience seizures or other symptoms of this problem, you need to get serious treatment. If you let everything take its course, the risk of a sad outcome will increase significantly.

Chapter 11. Paroxysmal disorders

Paroxysms are short-term, suddenly occurring and abruptly ending disorders that are prone to reappearance. A variety of mental (hallucinations, delirium, confusion, attacks of anxiety, fear or drowsiness), neurological (convulsions) and somatic (palpitations, headaches, sweating) disorders can occur paroxysmally. In clinical practice, the most common cause of paroxysms is epilepsy, but paroxysms are also characteristic of some other diseases, for example, migraine (see section 12.3) and narcolepsy (see section 12.2).

11.1. Epileptiform paroxysms

Epileptiform paroxysms include short-term attacks with a wide variety of clinical pictures, directly related to organic brain damage. Epileptiform activity can be detected on the EEG in the form of single and multiple peaks, single and rhythmically repeating (frequency 6 and 10 per second) sharp waves, short-term bursts of high-amplitude slow waves and especially peak-wave complexes, although these phenomena are also recorded in people without clinical signs of epilepsy.

There are many classifications of paroxysms depending on the location of the lesion (temporal, occipital lesions, etc.), age of onset (childhood epilepsy - pycnolepsy), causes of occurrence (symptomatic epilepsy), and the presence of seizures (convulsive and non-convulsive paroxysms). One of the most common classifications is the division of seizures according to leading clinical manifestations.

Big seizure ( grand mal ) manifests itself as a sudden loss of consciousness with a fall, a characteristic change of tonic and clonic convulsions and subsequent complete amnesia. The duration of a seizure in typical cases ranges from 30 seconds to 2 minutes. The patients' condition changes in a certain sequence. Tonic phase manifested by sudden loss of consciousness and tonic convulsions. Signs of loss of consciousness are loss of reflexes, reactions to extraneous stimuli, and lack of pain sensitivity (coma). As a result, patients falling cannot protect themselves from serious injuries. Tonic convulsions are manifested by a sharp contraction of all muscle groups and a fall. If there was air in the lungs at the time of the seizure, a sharp cry is observed. With the onset of the attack, breathing stops. The face first turns pale, and then cyanosis increases. The duration of the tonic phase is 20-40 s. Klonichva phase also occurs against the background of switched off consciousness and is accompanied by simultaneous rhythmic contraction and relaxation of all muscle groups. During this period, urination and defecation are observed, the first respiratory movements appear, but full breathing is not restored and cyanosis persists. The air expelled from the lungs forms foam, sometimes stained with blood due to biting the tongue or cheek. The duration of the tonic phase is up to 1.5 minutes. The attack ends with the restoration of consciousness, but for several hours after this, somnolence is observed. At this time, the patient can answer simple questions from the doctor, but, left to his own devices, falls asleep deeply.

In some patients, the clinical picture of a seizure may differ from the typical one. Often one of the phases of seizures is absent (tonic and clonic seizures), but the reverse sequence of phases is never observed. In approximately half of cases, the onset of seizures is preceded by aura(various sensory, motor, visceral or mental phenomena, extremely short-term and identical in the same patient). Clinical features of the aura may indicate the localization of the pathological focus in the brain (somatomotor aura - posterior central gyrus, olfactory - uncinate gyrus, visual - occipital lobes). Some patients, several hours before the onset of a seizure, experience an unpleasant feeling of weakness, malaise, dizziness, and irritability. These phenomena are called warning signs of a seizure.

Minor seizure ( petit mal ) - short-term loss of consciousness followed by complete amnesia. A typical example of a petit mal seizure is absence seizure, during which the patient does not change position. Switching off consciousness is expressed in the fact that he stops the action he has started (for example, he becomes silent in a conversation); the gaze becomes “floating”, meaningless; the face turns pale. After 1-2 seconds, the patient comes to his senses and continues the interrupted action, not remembering anything about the seizure. No convulsions or falls are observed. Other variants of petit mal seizures - complex absence seizures, accompanied by abortive convulsive movements forward (propulsion) or back (retropulsions), tilts like an eastern greeting (salaam-fits). In this case, patients may lose their balance and fall, but immediately get up and regain consciousness. Petite seizures are never accompanied by an aura or warning signs.

Nonconvulsive paroxysms, equivalent to seizures, are of great difficulty for diagnosis. The equivalents of seizures can be twilight states, dysphoria, and psychosensory disorders.

Twilight states - suddenly arising and suddenly ending disorders of consciousness with the possibility of committing quite complex actions and actions and subsequent complete amnesia. Twilight states are described in detail in the previous chapter (see section 10.2.4).

In many cases, epileptiform paroxysms are not accompanied by loss of consciousness and complete amnesia. An example of such paroxysms are dysphoria - sudden attacks of altered mood with a predominance of angry-sad affect. Consciousness is not darkened, but affectively narrowed. Patients are agitated, aggressive, react angrily to remarks, show dissatisfaction in everything, express themselves sharply offensively, and can hit their interlocutor. After the attack is over, patients calm down. They remember what happened and apologize for their behavior. A paroxysmal occurrence of pathological desires is possible: thus, epileptiform activity is manifested in periods of excessive drinking - dipsomania. Unlike patients with alcoholism, such patients do not experience a pronounced craving for alcohol outside of an attack and drink alcohol in moderation.

Almost any symptom of productive disorders can be a manifestation of paroxysms. Occasionally, paroxysmal hallucinatory episodes, unpleasant visceral sensations (senestopathies) and attacks with primary delirium occur. Quite often during attacks, the psychosensory disorders and episodes of derealization described in Chapter 4 are observed.

Psychosensory seizures manifested by the feeling that surrounding objects have changed size, color, shape or position in space. Sometimes you get the feeling that parts of your own body have changed (“ body schema disorders"). Derealization and depersonalization during paroxysms can be manifested by attacks of dejavu and jamaisvu. It is characteristic that in all these cases the patients retain fairly detailed memories of painful experiences. The memory of real events at the time of the seizure is somewhat worse: patients can only remember fragments from the statements of others, which indicates an altered state of consciousness. M. O. Gurevich (1936) proposed to distinguish such disorders of consciousness from typical syndromes of switching off and clouding of consciousness and designated them as "special states of consciousness".

A 34-year-old patient has been seen by a psychiatrist since infancy due to mental retardation and frequent paroxysmal attacks. The cause of organic brain damage is otogenic meningitis suffered in the first year of life. Over the past years, seizures occur 12-15 times a day and are characterized by stereotypic manifestations. A few seconds before the onset, the patient can sense the approach of an attack: suddenly he grabs his right ear with his hand, holds his stomach with the other hand, and after a few seconds raises it to his eyes. Doesn't answer questions, doesn't follow doctor's instructions. After 50-60 seconds the attack passes. The patient reports that at this time he smelled tar and heard a rude male voice in his right ear, uttering threats. Sometimes, simultaneously with these phenomena, a visual image appears - a white man, whose facial features cannot be seen. The patient describes in some detail the painful experiences during the attack, and also states that he felt the doctor’s touch at the time of the attack, but did not hear the speech addressed to him.

In the described example, we see that, in contrast to minor seizures and twilight stupefactions, the patient retains memories of the attack he suffered, but the perception of reality, as one would expect in special states of consciousness, is fragmentary and unclear. Phenomenologically, this paroxysm is very close to the aura preceding a grand mal seizure. Such phenomena indicate the local nature of the attack and the preservation of normal activity in other parts of the brain. In the described example, the symptoms correspond to the temporal localization of the lesion (the anamnesis data confirms this point of view).

The presence or absence of focal (focal) manifestations is the most important principle of the International Classification of Epileptiform Paroxysms (Table 11.1). In accordance with the International Classification, seizures are divided into generalized(idiopathic) and partial(focal). Electroencephalographic examination is of great importance for the differential diagnosis of these types of paroxysms. Generalized seizures correspond to the simultaneous appearance of pathological epileptic activity in all parts of the brain, while with focal seizures, changes in electrical activity occur in one focus and only later can affect other parts of the brain. There are also clinical signs characteristic of partial and generalized seizures.

Generalized seizures always accompanied by a severe disorder of consciousness and complete amnesia. Since a seizure immediately disrupts the functioning of all parts of the brain at the same time, the patient cannot feel the approach of an attack, and an aura is never observed. A typical example of generalized seizures are absence seizures and other types of minor seizures.

Table 11.1. International classification of epileptic paroxysms

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29. Syndromes of impaired consciousness. Paroxysmal clouding of consciousness. Syndromes of impaired consciousness.

29. Syndromes of impaired consciousness. Paroxysmal clouding of consciousness.

Syndromes of impaired consciousness.

Disorders of consciousness are divided by structure - switching off (non-psychotic or quantitative disturbances of consciousness) and stupefaction (psychotic or qualitative disturbances of consciousness) and by dynamics - paroxysmal and non-paroxysmal arising. The following variants of syndromes of impaired consciousness are distinguished: non-paroxysmal - stupor: delirium, oneiroid, amentia: switching off: stupor, stupor, coma; and paroxysmal - stupefaction: twilight states of consciousness, special states of consciousness, aura of consciousness; switching off - large and small convulsions.

Switching off consciousness is a total disruption of reflective mental activity, which consists of a consistent or immediate decrease in volume and depth, up to the complete disappearance of mental functioning. The sequential development of quantitative impairment of consciousness is described below. Syndromes of switching off consciousness belong to urgent medicine and require urgent qualified medical care, since when they increase, they are accompanied by cardiovascular, respiratory and cerebral disorders and can lead to death.

Confusion of consciousness is a total disintegration of all mental activity, including as leading symptoms the general signs of K. Jaspers - disorientation in time, situation, place, one’s own personality: detachment from the real world, disorders of comprehension and congenital memory impairment. Almost all psychopathological symptoms occur as additional symptoms: hypo- and hyperesthesia, senestopathy, illusions, hallucinations, psychosensory disorders, delusions, false recognitions and memories, vivid affective disorders (anxiety, fear, euphoria, depression, indifference), various psychomotor symptoms ( agitation, stupor, speech disorders), memory disorders. In contrast to the switching off of consciousness, during stupefaction there is a fragmentary reflection of objective reality, mixed with qualitative mental disorders.

Non-paroxysmal development of disturbances of consciousness is characterized by a sequential stage-by-stage change in the depth and volume of disturbances of consciousness, both switching off (stunning - stupor - coma) and stupefaction (for example, stage 3 of the development of delirium). Development can be different in speed: acute, subacute, chronic. In addition, non-paroxysmal disturbances of consciousness are characterized by a longer duration of symptoms.

Paroxysmal development of disturbances of consciousness occurs suddenly, with the absence of stages in their development. The painful state occurs suddenly, immediately in an expanded form, capturing all the mental activity of the patient, lasting from several seconds, minutes, rarely days, months.

Paroxysmal clouding of consciousness.

Twilight stupefaction is an acute stupefaction of consciousness, in which there is deep disorientation in time, surroundings and one’s own personality (leading symptoms) in combination with hallucinatory and delusional statements, an affect of melancholy, anger and fear, sharp hallucinatory-delusional excitement, incoherent speech, less often with outwardly ordered behavior (optional symptoms). Upon recovery from this syndrome, there is complete total congrade amnesia, less often of a retarded nature.

There are organic (classical) and hysterical twilight stupefactions.

In the classic twilight state of consciousness, in addition to the leading symptoms described above, there is a full set of optional symptoms. Based on their severity, hallucinatory, delusional and dysphoric variants are distinguished. Classic twilight stupefaction, especially the dysphoric variant with frantic agitation, poses an increased social danger.

Ambulatory automatism (twilight state of consciousness with automatism). Unlike classic twilight stupefaction, there are no optional symptoms (delusions, hallucinations, dysphoria). Automatic, often quite complex motor acts are noted against the background of an impassive affect with a tinge of some confusion.

Fugues are motor automatisms when patients wander aimlessly, walk, run aimlessly, etc.

Trance is a special automatism when outwardly complex sequential actions seem correct, orderly, purposeful, but are actually meaningless, unnecessary and not planned by the patient. In this connection, only careful observation reveals some confusion, detachment, and mutism.

All variants of twilight states can occur not only during the day, but also at night (somnambulism - sleepwalking, sleepwalking).

Organic twilight states of consciousness occur in epilepsy and organic diseases of the brain.

Hysterical twilight states are psychogenically arising peculiar disorders of consciousness, when against the background of selective disorientation with preservation of partial contact with the patient, an influx of vivid hallucinations, unsystematized delusional ideas and theatrically pathetic scenes (twilight state with the affect of grief, despair and anger).

There are also hysterical ambulatory automatisms (rather complex, habitual, ordinary actions) and fugues (purposeless, outwardly expedient sudden actions, for example, flight, stupor).

Pseudo-dementia is a narrowing of consciousness, when patients are confused, helpless, stupid, stare, answer inappropriately, stupidly and dementiatically, as if they have lost the simplest skills and basic knowledge. Depressive and agitated forms are distinguished based on optional symptoms. Ganser syndrome is very closely related, where in addition to “dementia” behavior, “dementia” responses are also observed.

Puerilism is characterized by a kind of regression of behavior to childhood, when an adult behaves like a child with childish manners, gestures, games, pranks, and intonations. Along with childish behavior in answers, individual habits, skills and statements of an adult are less often retained in behavior.

Pathological affect is an affectively determined twilight state of consciousness, accompanied by destructive actions and complete amnesia of what was experienced in a painful state.

Fugiform reactions are psychogenically caused twilight states of consciousness, expressed by meaningless flight.

Occurs in hysteria, hysterical psychopathy, affective-shock reactions, and exceptional conditions.

Special states of consciousness are manifested by a superficial change in consciousness with signs of depersonalization and derealization, confusion, disorientation in time, situation, environment while retaining memories of the experience.

Aura of consciousness is a short-term clouding of consciousness with disorientation in time, surroundings and retention of memories of painful experiences, which can be represented by psychosensory disorders, depersonalization, derealization, phenomena of “already seen”, “never seen”, true hallucinations, affective disorders.

Occurs in epilepsy and organic brain diseases.

Fainting

Fainting

Fainting (syncope) is a suddenly developing pathological condition characterized by a sharp deterioration in well-being, painful experiences of discomfort, increasing weakness, vegetative-vascular disorders, decreased muscle tone and usually accompanied by a short-term disturbance of consciousness and a fall. Fainting is the most common form of paroxysmal disorders of consciousness, occurring equally often in men and women, mainly in young and mature adults.

Etiology and pathogenesis. The occurrence of fainting is associated with an acute metabolic disorder of brain tissue due to deep hypoxia (see full body of knowledge) or the occurrence of conditions that impede the utilization of oxygen by brain tissue (see full body of knowledge Hypoglycemia).

In most cases, fainting has a reflex neurogenic origin associated with congenital or acquired characteristics of the body.

Fainting can be caused by the influence of various factors that cause transient spasm of cerebral vessels, including negative emotions due to fear, an unpleasant sight, a conflict situation (psychogenic Fainting); pain (painful fainting); the use of certain medications, for example, ganglion blockers; irritation of certain receptor zones, for example, the sinocarotid region (sinocarotid Syncope), the vagus nerve (vasovagal Syncope), the vestibular apparatus and others. The pathogenic cerebral vascular effects that arise in this case are often associated with bradycardia and a drop in blood pressure. In the origin of vasovagal syncope, importance is also attached to central parasympathetic influences.

Fainting can be a consequence of disturbances in adaptive mechanisms in diseases of the brain that affect suprasegmental vegetative formations, as well as in functional disorders that occur in practically healthy individuals, but are temporarily weakened as a result of exposure to adverse environmental factors, endogenous or exogenous intoxications, malnutrition, lack of sleep, significant overwork. Fainting in these individuals more often occurs due to the action of these factors with a sharp increase in motor, mental and emotional activity.

Fainting can occur when standing motionless for a long time or quickly getting up from a horizontal position, especially after a night's sleep (orthostatic fainting), as well as during significant physical effort (cross country, overcoming an obstacle course, etc.) and intense mental activity, accompanied by emotional stress.

Hypoxia of brain tissue or disorders of cerebral metabolism of another origin, developing in certain diseases and pathological conditions; standing, are the cause of the so-called symptomatic fainting. These fainting are often caused by disturbances of cardiac activity - rhythm changes such as Morgagni-Adams-Stokes syndrome, heart valve defects, decreased contractile function of the myocardium, coronary heart disease; arterial hypotension and hypertensive crises, collaptoid reactions (see full body of knowledge Collapse); vegetative-vascular paroxysms in allergic conditions and endocrine-hormonal dysfunctions, hypothalamic crises, migraines; disorders of cerebral circulation in organic diseases of the brain and its vessels (tumors, hypertensive-hydrocephalic syndromes, atherosclerosis, cerebral vasculitis and others); occlusions, stenoses and deformation of the main vessels supplying the brain; periodic vertebrobasilar vascular insufficiency (Unterharnscheidt syndrome); blood diseases in which oxygen transport deteriorates; hypoglycemic conditions, external respiration disorders.

In some cases, Fainting is caused by extreme environmental influences - lack of oxygen in the inhaled air (see full body of knowledge Altitude sickness), acceleration in the pelvis-head direction that occurs on an airplane, in an elevator, and so on (see full body of knowledge Acceleration).

Clinical picture. Fainting has three sequential stages - precursors (presyncope), disturbances of consciousness and the recovery period.

The precursor stage begins with subjective feelings of discomfort, increasing weakness, dizziness, nausea, discomfort in the heart and abdomen and ends with darkening in the eyes, the appearance of noise or ringing in the ears, a narrowing of the scope of attention, a feeling of the ground floating from under one’s feet, or sinking. Objectively, pronounced vegetative-vascular disorders are observed - pallor of the skin and visible mucous membranes, instability of pulse, respiration and blood pressure, hyperhidrosis and decreased muscle tone. This stage lasts several seconds (rarely up to a minute), and patients usually have time to complain about deterioration in health, and sometimes even lie down and take the necessary medications, which in some cases can prevent further development of fainting

With the unfavorable development of Fainting, the general condition continues to rapidly deteriorate, a sharp pallor of the skin occurs, a deep decrease in muscle tone, including postural, the patient falls, sometimes trying to hold on to surrounding objects. Consciousness is impaired, the depth and duration of disorders of consciousness may vary. In the case of an abortive course, fainting can only occur in a short-term, partial narrowing of consciousness, disorientation or moderate stupor. With mild fainting, consciousness is lost for several seconds, with deep fainting - for several minutes (in rare cases, up to 30-40 minutes). During the period of loss of consciousness, patients do not make contact, their body is motionless, their eyes are closed, the pupils are dilated, their reaction to light is slow, the corneal reflex is absent, the pulse is weak, barely detectable, often rare, breathing is shallow, blood pressure is reduced (less than 95/ 55 millimeters of mercury), muscles are relaxed. Deep fainting may be accompanied by short-term convulsions of a tonic, less often clonic nature. Restoration of consciousness occurs within a few seconds.

Complete restoration of function and normalization of well-being takes from several minutes to several hours, depending on the severity of the experience. Fainting (recovery period). There are no symptoms of organic damage to the nervous system.

The diagnosis is made on the basis of clinical pictures. Differential diagnosis is carried out with epileptic and hysterical seizures (see full body of knowledge Hysteria, Epilepsy), collapse (see full body of knowledge). Differential diagnostic signs: Fainting occurs in a certain situation, mainly in an upright position of the body; with fainting, a clinically pronounced period of precursors is observed, a slow rate of fall and loss of consciousness, decreased muscle tone, rapid recovery of consciousness after taking measures to improve cerebral circulation, and the absence of amnesia.

Treatment is aimed at improving blood supply and oxygenation to the brain. The patient should be placed in a horizontal position with his head down and legs raised, provide access to fresh air, free from restrictive clothing, sprinkle cold water on his face, and pat his cheeks. If this is not enough, inhalation of ammonia, injections of cordiamine and caffeine are indicated.

In severe cases, when fainting persists, indirect cardiac massage is indicated (see full body of knowledge) and mouth-to-mouth artificial respiration (see full body of knowledge Artificial respiration). In case of cardiac arrhythmia, antiarrhythmic drugs are used. For symptomatic fainting, treatment is aimed at eliminating the cause that caused it. In cases where syncope is caused by Morgagni syndrome -

Adams-Stokes, atropine injections, ephedrine administration, sublingual administration of isadrin or novodrinum in the form of inhalations are prescribed. If these measures are ineffective, it is necessary (in a clinical setting) to connect an electrical pacemaker (see the full body of knowledge Cardiac pacing). Fainting that occurs in flight due to the effects of overloads is stopped when the aircraft is transferred to a straight flight path. If signs of high-altitude fainting occur during tests in a pressure chamber, it is necessary to “descent” to normal atmospheric pressure at the maximum technically possible speed and at the same time provide oxygen inhalation.

Paroxysmal disorders of consciousness caused by hypoglycemic conditions are relieved by parenteral administration of glucose.

The prognosis depends on the reasons that caused Fainting and the timeliness of assistance. In most cases it is favorable, but in some cases (high-altitude Fainting) it can be unfavorable if emergency measures are not taken in a timely manner.

Paroxysmal disorders

Paroxysmal disorders of consciousness in neurology are a pathological syndrome that occurs as a result of the course of the disease or the body’s reaction to an external stimulus. Disorders manifest themselves in the form of attacks (paroxysms) of various types. Paroxysmal disorders include migraine attacks, panic attacks, fainting, dizziness, epileptic seizures with and without convulsions.

Neurologists at the Yusupov Hospital have extensive experience in treating paroxysmal conditions. Doctors know modern effective methods for treating neurological pathologies.

Paroxysmal disorder of consciousness

Paroxysmal disorder of consciousness manifests itself in the form of neurological attacks. It can occur against the background of apparent health or during an exacerbation of a chronic disease. Often, paroxysmal disorder is recorded during the course of a disease that is not initially associated with the nervous system.

The paroxysmal state is characterized by the short duration of the attack and the tendency to recur. The disorder has different symptoms, depending on the provoking condition. Paroxysmal disorder of consciousness can manifest itself as:

• epileptic seizure,
• fainting,
• sleep disorder,
• panic attack,
• paroxysmal headache.

The causes of the development of paroxysmal conditions can be congenital pathologies, injuries (including at birth), chronic diseases, infections, and poisoning. Patients with paroxysmal disorders often have a hereditary predisposition to such conditions. Social conditions and harmful working conditions can also cause the development of pathology. Paroxysmal disorders of consciousness can cause:

• bad habits (alcoholism, smoking, drug addiction);
• stressful situations (especially when they are repeated frequently);
• disturbance of sleep and wakefulness;
• heavy physical activity;
• prolonged exposure to loud noise or bright light;
• unfavorable environmental conditions;
• toxins;
• sudden change in climatic conditions.

Paroxysmal disorders in epilepsy

In epilepsy, paroxysmal conditions can manifest themselves in the form of convulsive seizures, absence seizures and trances (non-convulsive paroxysms). Before a grand mal seizure occurs, many patients feel a certain type of warning sign - the so-called aura. There may be auditory, auditory and visual hallucinations. Someone hears a characteristic ringing or feels a certain smell, feels a tingling or tickling sensation. Convulsive paroxysms in epilepsy last several minutes and may be accompanied by loss of consciousness, temporary cessation of breathing, involuntary defecation and urination.

Nonconvulsive paroxysms occur suddenly, without warning. With absence seizures, a person suddenly stops moving, his gaze is directed ahead, he does not react to external stimuli. The attack does not last long, after which mental activity returns to normal. The attack goes unnoticed by the patient. Absence seizures are characterized by a high frequency of attacks: they can be repeated tens or even hundreds of times per day.

Panic disorder (episodic paroxysmal anxiety)

Panic disorder is a mental disorder in which the patient experiences spontaneous panic attacks. Panic disorder is also called episodic paroxysmal anxiety disorder. Panic attacks can occur from several times a day to once or twice a year, while the person is constantly expecting them. Severe anxiety attacks are unpredictable because their occurrence does not depend on the situation or circumstances.

This condition can significantly impair a person's quality of life. The feeling of panic can be repeated several times a day and last for an hour. Paroxysmal anxiety can occur suddenly and cannot be controlled. As a result, a person will feel discomfort while in society.

Paroxysmal sleep disorders

The manifestations of paroxysmal sleep disorders are very diverse. These may include:

• nightmares;
• talking and screaming in sleep;
• sleepwalking;
• motor activity;
• night cramps;
• shuddering when falling asleep.

Paroxysmal sleep disorders do not allow the patient to regain strength or rest properly. After waking up, a person may feel headaches, fatigue and weakness. Sleep disorders are common in patients with epilepsy. People with this diagnosis often have realistic, vivid nightmares in which they run somewhere or fall from a height. During nightmares, your heart rate may increase and you may perspire. Such dreams are usually remembered and can be repeated over time. In some cases, during sleep disorders, breathing disturbance occurs; a person may hold his breath for a long period of time, and there may be erratic movements of the arms and legs.

Treatment of paroxysmal disorders

To treat paroxysmal conditions, consultation with a neurologist is necessary. Before prescribing treatment, the neurologist must know exactly the type of attacks and their cause. To diagnose the condition, the doctor clarifies the patient’s medical history: when the first episodes of attacks began, under what circumstances, what their nature is, and whether there are any concomitant diseases. Next, you need to undergo instrumental studies, which may include EEG, EEG video monitoring, MRI of the brain and others.

After performing an in-depth examination and clarifying the diagnosis, the neurologist selects treatment strictly individually for each patient. Therapy for paroxysmal conditions consists of medications in certain doses. Often the dosage and the drugs themselves are selected gradually until the required therapeutic effect is achieved.

Typically, treatment of paroxysmal conditions takes a long period of time. The patient should be constantly monitored by a neurologist for timely adjustment of therapy if necessary. The doctor monitors the patient’s condition, assesses the tolerability of the drugs and the severity of adverse reactions (if any).

The Yusupov Hospital has a staff of professional neurologists who have extensive experience in treating paroxysmal conditions. Doctors are proficient in modern effective methods of treating neurological pathologies, which allows them to achieve great results. The Yusupov Hospital performs diagnostics of any complexity. Using high-tech equipment, which facilitates the timely start of treatment and significantly reduces the risk of complications and negative consequences.

The clinic is located near the center of Moscow and receives patients around the clock. You can make an appointment and get advice from specialists by calling the Yusupov Hospital.

Paroxysmal states. Fainting

Fainting, or syncope, is an attack of short-term loss of consciousness and impaired muscle tone of the body (fall) due to a disorder of cardiovascular and respiratory activity. Syncope conditions can be neurogenic in nature (psychogenic, irritative, maladaptive, dyscirculatory), develop against the background of somatic pathology (cardiogenic, vasodepressor, anemic, hypoglycemic, respiratory), under extreme influences (hypoxic, hypovolemic, intoxication, medication, hyperbaric). Syncope, despite its short duration, is a process unfolding over time, in which successive stages can be distinguished: precursors (presyncope), peak (syncope itself) and recovery (postsyncope). The severity of clinical manifestations and the duration of each of these stages are very diverse and depend mainly on the pathogenetic mechanisms of fainting.

Fainting can be provoked by an upright position, stuffiness, various stressful situations (unpleasant news, blood drawing), sudden acute pain. In some cases, fainting occurs for no apparent reason. Fainting can occur from once a year to several times a month.

Clinical manifestations. Immediately after the provoking situation, a presyncope (lipothymic) state develops, lasting from several seconds to several minutes. At this stage, severe general weakness, unsystematic dizziness, nausea, flickering of “spots”, “veils” before the eyes are observed, these symptoms quickly increase, there is a premonition of a possible loss of consciousness, noise or ringing in the ears. Objectively, during the lipothymic period, pallor of the skin, local or general hyperhidrosis, decreased blood pressure, pulse instability, respiratory arrhythmia are noted, coordination of movements is impaired, and muscle tone decreases. The paroxysm can end at this stage or move into the next stage - the actual syncope state, in which all the described symptoms increase, the patients fall, and consciousness is impaired. The depth of loss of consciousness varies from slight stupefaction to deep disturbance lasting several minutes. During this period, there is a further decrease in blood pressure, shallow breathing, the muscles are completely relaxed, the pupils are dilated, their reaction to light is slow, and tendon reflexes are preserved. With a deep loss of consciousness, short-term convulsions, often tonic, and involuntary urination may develop. In the post-syncope period, the restoration of consciousness occurs quickly and completely, patients immediately orient themselves in the environment and what happened, and remember the circumstances preceding the loss of consciousness. The duration of the post-syncope period ranges from several minutes to several hours. During this period of time, general weakness, non-systemic dizziness, dry mouth are noted, pale skin remains, hyperhidrosis, decreased blood pressure, and uncertainty of movements.

Diagnosis diagnosed on the basis of a carefully collected anamnesis, examination of somatic and neurological status; all patients with syncope are required to undergo echocardiography, VEM, Echo-CG, 24-hour blood pressure monitoring, EEG, ultrasound, radiography of the cervical spine, EEG and EEG monitoring

United treatment plan It is difficult to recommend patients in the interictal period, since the causes and pathogenetic mechanisms of the development of various variants of syncope are very diverse. Treatment is prescribed only after a thorough examination of the patient and substantiation of the diagnosis not only of the underlying disease, but also clarification of the leading pathogenetic mechanisms of the development of fainting.

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Paroxysms are short-term, suddenly occurring and abruptly ending disorders that are prone to reappearance. A variety of mental (hallucinations, delirium, confusion, attacks of anxiety, fear or drowsiness), neurological (convulsions) and somatic (palpitations, headaches, sweating) disorders can occur paroxysmally. In clinical practice, the most common cause of paroxysms is epilepsy.

Epileptic and epileptiform seizures– a manifestation of organic brain damage, as a result of which the entire brain or its individual parts are involved in pathological rhythmic activity, recorded in the form of specific complexes on the EEG. Pathological activity may include loss of consciousness, seizures, episodes of hallucinations, delusions, or bizarre behavior.

Characteristic signs of epileptic and epileptiform paroxysms:

Spontaneity (absence of provoking factors);

Sudden onset;

Relatively short duration (seconds, minutes, sometimes tens of minutes);

Sudden cessation, sometimes during sleep phase;

Stereotyping and repetition.

The specific symptoms of a seizure depend on which parts of the brain are involved in the pathological activity. It is customary to divide seizures into generalized And partial (focal). Generalized seizures, in which all parts of the brain are simultaneously subject to pathological activity, manifested by a complete loss of consciousness, sometimes by general convulsions. Patients have no memory of the seizure.

Partial (focal) seizures do not lead to complete loss of consciousness, patients retain individual memories of the paroxysm, pathological activity occurs only in one of the parts of the brain. Thus, occipital epilepsy is manifested by periods of blindness or flashes, flickering in the eyes, temporal epilepsy - by episodes of hallucinations (auditory, olfactory, visual), damage to the precentral gyrus - by unilateral convulsions in one of the limbs (Jacksonian seizures).

The partial nature of the seizure is also indicated by the presence of precursors (unpleasant sensations in the body that occur several minutes or hours before the attack) and an aura (a short initial phase of the seizure, which is stored in the patient’s memory). Doctors pay special attention to partial seizures because they may be the first manifestation of focal brain lesions, such as tumors.

Seizures are usually classified according to their main clinical manifestations.

Epileptic paroxysms include:

Grand mal seizures (grand mal, clonicotonic seizures);

Minor seizures (petit mal, simple and complex absences, myoclonic seizures);

Twilight stupefactions (outpatient automatisms, somnambulism, trances, hallucinatory-delusional variant);

Dysphoria;

Special states of consciousness (psychosensory seizures, attacks of “déjà vu” and “jamais vu”, paroxysms of delusional and hallucinatory structure);

Jacksonian seizures with convulsions in one of the limbs.

Big convulsive seizure (grand mal)

manifests itself as a sudden loss of consciousness with a fall, a characteristic change of tonic and clonic convulsions and subsequent complete amnesia. The duration of the attack is from 30 s to 2 minutes. The patients' condition changes in a certain sequence. The tonic phase is replaced by a clonic phase and the seizure ends with the restoration of consciousness, but for several hours after this, somnolence is observed. At this time, the patient can answer simple questions from the doctor, but, left to his own devices, falls asleep deeply.

In approximately half of the cases, the occurrence of seizures is preceded by an aura (various sensory, motor, visceral or mental phenomena, extremely short-lived and identical in the same patient). Some patients, several hours before the onset of a seizure, experience an unpleasant feeling of weakness, malaise, dizziness, and irritability. These phenomena are called seizure warning signs.

A minor seizure (petit mal) is a short-term loss of consciousness followed by complete amnesia. A typical example of a minor seizure is absence seizure, during which the patient does not change position. Switching off consciousness is expressed in the fact that he stops the action he has started (for example, he becomes silent in a conversation); the gaze becomes “floating”, meaningless; the face turns pale. After 1-2 seconds, the patient comes to his senses and continues the interrupted action, not remembering anything about the seizure. No convulsions or falls are observed. Petite seizures are never accompanied by an aura or warning signs.

Nonconvulsive paroxysms, equivalent to seizures, are of great difficulty for diagnosis. The equivalents of seizures can be twilight states, dysphoria, and psychosensory disorders.

Twilight states are suddenly occurring and suddenly ending disorders of consciousness with the possibility of performing rather complex actions and deeds and subsequent complete amnesia. In many cases, epileptiform paroxysms are not accompanied by loss of consciousness and complete amnesia. An example of such paroxysms is dysphoria - sudden attacks of altered mood with a predominance of angry-sad affect. Consciousness is not darkened, but affectively narrowed. Patients are agitated, aggressive, react angrily to remarks, show dissatisfaction in everything, express themselves sharply offensively, and can hit their interlocutor. After the attack is over, patients calm down. They remember what happened and apologize for their behavior. Almost any symptom of productive disorders can be a manifestation of paroxysms.

Related information.

Myakotnykh V.S.
(educational manual)

There are several variants of predominantly non-epileptic paroxysmal disorders that require special consideration and are quite common in the clinic of nervous diseases. These conditions are divided into several of the most common variants, the clinical description of which is difficult to find in any one textbook or monograph. Basically they can be divided into:

1. Dystonia or muscle dystonic syndromes
2. Myoclonic syndromes and a number of other hyperkinetic conditions
3. Headache
4. Autonomic disorders

Often, the clinical manifestation of these pathological conditions is associated with a neurological nosology that occurs in young (childhood, adolescence, youth) age. But, as practice shows, in adults and even the elderly, the described syndromes very often either debut or progress, the appearance and severity of which is associated with age-related cerebral disorders, acute and chronic cerebrovascular accidents. It should be noted that many non-epileptic paroxysmal conditions can also be a consequence of long-term use of various medications used to treat circulatory failure, some mental disorders of the elderly and senile, parkinsonism, etc. Therefore, in this publication we do not strive to present the identified pathological conditions in the form of syndromes occurring in a certain nosology, and even more so, in the form of individual nosological units. Let us dwell on the most common variants of non-epileptic paroxysms highlighted above.

I. Dystonia.

Dystonia is manifested by constant or periodic muscle spasms, leading to “dystonic” postures. In this case, of course, we are not talking about the well-known concepts of vegetative-vascular or neurocirculatory dystonia, which are considered completely separately.

Epidemiology. Dystonia is a rare disease: the incidence of its various forms is 300-400 patients per 1 million people (0.03%). Generalized dystonia can be inherited dominantly or recessively. The genetic mechanisms of focal dystonias are unknown, although it has been noted that about 2% of focal dystonias are inherited, and a third of patients with blepharospasm and spasmodic torticollis had other movement disorders (tics, tremor, etc.) in their families.

The pathogenetic mechanisms of dystonia still remain unsolved. Dystonia does not have a clear morphological substrate in the brain and is caused by subcellular and neurodynamic disorders in certain brain systems. The peripheral motor apparatus, the pyramidal tract, and the proprioceptive servo mechanism (stretch reflex) are intact in dystonia. Disturbances in the functional state of interneurons of the brain stem and spinal cord were revealed.

Also, the biochemical defect underlying dystonia is almost unknown. Empirically, it can be assumed that the cholinergic, dopaminergic and GABAergic systems of the brain are involved. But the low effectiveness of treatment for dystonia in general suggests the existence of some other, still unknown, biochemical disorders underlying the disease. Most likely, the trigger that triggers dystonia is the biochemical systems at the level of the oral part of the brain stem and its connections with the subcortical extrapyramidal formations (mainly the putamen, thalamus optica, and others).

Depending on the distribution of hyperkinesis across muscle groups and the degree of generalization, 5 forms of dystonia and dystonic syndromes are distinguished:

1. focal dystonia,
2. segmental dystonia,
3. hemidystonia,
4. generalized and
5. multifocal dystonia.

Focal dystonia is characterized by the involvement of the muscles of any one part of the body (“writer’s cramp”, “blepharospasm”, etc.).

Segmental dystonia is manifested by the involvement of two adjacent parts of the body (orbicularis oculi and orbicularis oris; neck and arms; pelvic girdle and legs, etc.).

With hemidystonia, involvement of the muscles of one half of the body is observed (arms and legs most often). Such dystonia is often symptomatic and directs the doctor to a diagnostic search for the primary lesion of the nervous system.

Generalized dystonia is characterized by involvement of muscles throughout the body.

Multifocal dystonia affects two or more non-contiguous areas of the body (for example, blepharospasm and foot dystonia; torticollis and writer's cramp, etc.).

Focal dystonias are much more common than generalized dystonias and have six main and relatively independent forms:

• blepharospasm,
• oromandibular dystonia,
• spasmodic dysphonia,
• spastic torticollis,
• writer's cramp,
• foot dystonia.

Generalized dystonia usually begins with focal dystonic disorders; its debut often occurs in childhood and adolescence. The older age focal dystonia begins, the less likely its subsequent generalization.

Postures and syndromes characteristic of dystonia are presented in Table 1.

But the division of dystonia into focal and generalized reflects only the syndromic principle of classification. The formulation of the diagnosis must also include the nosological principle - the name of the disease. The most complete nosological classification of dystonia is presented in the international classification of extrapyramidal disorders (1982), as well as in a general article by McGuire (1988). These classifications distinguish between primary and secondary forms of dystonia. In primary forms, dystonia is the only neurological manifestation. They can be either hereditary or sporadic. Secondary dystonias occur in cases of known and diagnosed diseases of the nervous system and are usually accompanied by other neurological disorders. In children, this occurs against the background of cerebral palsy (CP), Wilson's disease, and storage diseases; in adults, including the elderly - as a result of cerebral infarction, tumor, degenerative processes, use of medications, etc.

The defining characteristic of dystonia is the formation of typical dystonic postures, many of which have their own, sometimes figurative, names. The most typical dystonic postures and syndromes are given in Table 1 (cited from O.R. Orlova).

Since any area of ​​the body can be involved in dystonic hyperkinesis, the clinical pattern of dystonic syndrome in each individual patient depends on the distribution and combination of dystonic postures in different areas of the body. The modern convenient classification of dystonia (Marsden, 1987), given above, is based on this principle (the distribution of dystonic syndromes in different regions of the body).

It would be advisable to list the clinical features common to all focal dystonias.

Dystonic posture. With blepharospasm, closing, squinting of the eyes or frequent blinking is observed. Oromandibular dystonia is characterized by dystonic postures in the perioral region, tongue, and trismus. Spasmodic torticollis is manifested by rotation or tilting of the head. With writer's cramp, the posture of the hand resembles the “obstetrician’s hand.” Pathological postures that occur in the swallowing and voice-forming muscles during spastic dysphagia and dysphonia can be examined during a special ENT examination.

Action dystonia. In patients, the performance of certain actions performed by the muscles that form the dystonic posture is selectively impaired. With blepharospasm, the action is affected - keeping the eyes open, with spastic torticollis - keeping the head in a straight position, with writer's spasm, writing is impaired, with oromandibular dystonia, speech and eating may be impaired. In the case of spastic dysphagia and dysphonia, swallowing and voice are impaired. With ambulatory foot spasm, normal walking is disrupted. At the same time, other actions performed by the same muscle group are completely unimpaired. For example, a patient with writing cramp can perfectly use the “sick” hand in all everyday activities.

The dependence and variability of dystonia decreases with body position. As a rule, all manifestations of dystonia decrease or disappear when the patient lies down, and intensify when he stands.

The influence of the patient’s emotional and functional state on the severity of dystonia: reduction or disappearance of dystonia during sleep, in the morning after waking up, after drinking alcohol, in a state of hypnosis, the possibility of short-term volitional control, increased dystonia during stress and overwork. This feature is very clearly manifested at a doctor’s appointment, when during a 10-20 minute conversation all manifestations of dystonia may disappear, but as soon as the patient leaves the doctor’s office, they resume with renewed vigor. This feature can cause the doctor to mistrust the patient and suspect him of malingering.

Corrective gestures are special techniques that the patient uses to temporarily eliminate or reduce dystonic hyperkinesis. As a rule, this is either touching with your hand any point in the area of ​​interest, or simulating some kind of manipulation in this area. For example, patients with spasmodic torticollis, to reduce hyperkinesis, touch their cheek or any other point on the head with their hand, or imitate adjusting glasses, hairstyles, or a tie; patients with blepharospasm rub the bridge of their nose, take off and put on glasses; with oromandibular dystonia, chewing gum and sucking help for a short time sweets, as well as the presence of a stick, match, cigarette or any other object in the mouth. With writer's cramp, writing difficulties can be temporarily reduced if the healthy hand is placed on top of the “sick” one.

Paradoxical kinesis is a short-term reduction or elimination of hyperkinesis in the nature of the action (change in the locomotor stereotype). For example, patients with writer's cramp easily write with chalk on a blackboard, head rotation in patients with spasmodic torticollis may decrease or disappear when running or driving a car, in patients with spasmodic dysphonia the voice “cuts through” when singing or screaming, and in patients with ambulatory spasm of the foot, its pathological posture does not occur when walking on tiptoes or backwards.

Remissions are quite typical for focal dystonias. More often than with other forms, they are observed in patients with spastic torticollis (20-30%), when symptoms can spontaneously completely disappear for months and years, even several years after the onset of the disease. With exacerbation of spastic torticollis, the phenomenon of inversion of rotation is sometimes observed - a change in the direction of forced rotation of the head. Remissions are less typical for writer's cramp and other focal dystonias, however, with writer's cramp, the phenomenon of inversion is also observed - the transition of writer's cramp to the other hand.

A combination of focal forms of dystonia and the transition of one form to another. When two or more focal forms are combined, as a rule, the manifestations of one form predominate, while the others may be subclinical, and the symptoms of the erased form often appear before the symptoms of the clinically pronounced form. Example: Several years before the onset of spasmodic torticollis, about a third of patients experience difficulty writing or frequent blinking, but writer's cramp or blepharospasm is diagnosed after the onset of torticollis symptoms. There are cases when, after remission, one focal form is replaced by another, and one patient may have several such episodes. The classic combination is blepharospasm and oromandibular dystonia. In this case, blepharospasm usually appears first (the first stage of facial paraspasm) and is then joined by oromandibular dystonia (the second stage of facial paraspasm).

The dynamism of dystonia is most likely associated not with a specific anatomical substrate, which has not yet been discovered, but with a disruption of the interaction between the structures of the basal ganglia, brain stem, thalamus, limbic-reticular complex, motor cortex due to a violation of the exchange of neurotransmitters in these structures, which constitutes organic neurodynamic substrate of dystonia (Orlova O.R., 1989, 1997, 2001).

Diagnostic criteria of Marsden and Harrison (1975) for the diagnosis of idiopathic dystonia:

1. presence of dystonic movements or postures;
2. normal birth and early development;
3. absence of diseases or medications that could cause dystonia;
4. absence of paresis, oculomotor, atactic, sensory, intellectual disorders and epilepsy;
5. normal results of laboratory tests (copper metabolism, fundus, evoked potentials, electroencephalography, computed tomography and magnetic resonance imaging).

Spasmodic torticollis- the most common focal form of dystonia. The essence of dystonic syndrome in this case is a violation of keeping the head in a straight position, which is manifested by rotation or tilting of the head. Spasmodic torticollis usually begins at the age of 30 - 40 years, is 1.5 times more common in women, almost never generalizes, and can be combined with writer's cramp, blepharospasm and other focal dystonias. A third of patients experience remissions.

Writer's cramp. This form of dystonia occurs at the age of 20-30 years, equally often in men and women; Among the patients, people from “writing” professions predominate (doctors, teachers, lawyers, journalists) as well as musicians. Often, writer's cramp and its analogues (occupational dystonia) develop against the background of previous hand injuries or other pathology of the neuromotor system. Remissions from writing cramp are rare and, as a rule, short-lived.

Blepharospasm and oromandibular dystonia. These forms usually begin after the age of 45. As a rule, symptoms of oromandibular dystonia appear several years after the onset of blepharospasm.

Dystonia deserves special attention, manifested by sudden attacks of involuntary movements and pathological postures, which are never accompanied by a disturbance of consciousness and are often mistakenly regarded as hysterical or epileptic seizures. In some patients, attacks occur spontaneously, in others they are provoked by unprepared movements (kinotogenic or kinesigenic and non-kinetogenic or non-kinesigenic forms). Typical paroxysms: choreoathetotic, tonic or dystonic movements (generalized or hemitype), sometimes leading to the patient falling if he does not have time to grab onto any object. The attack lasts from several seconds to several minutes. Paroxysmal dystonia is either idiopathic (including familial) or symptomatic. The latter option is described for three diseases: cerebral palsy, multiple sclerosis and hypoparathyroidism. The drugs of choice for treatment are clonazepam, carbamazepine, and diphenine. The effect of treatment is high.

There is also a special form of dystonia that is sensitive to treatment with L-DOPA (Segawa disease). It responds very well to treatment with dopamine-containing drugs, and this is, perhaps, its main differential diagnostic criterion.

Treatment of dystonia. It is well known that there is no specific treatment for dystonia. This is due to the fact that neurochemical disorders in this disease are ambiguous, depend on the initial state of neurochemical systems and transform as the disease progresses. The most universal are GABAergic drugs (clonazepam and baclofen), however, previous treatment with drugs from other groups may reduce the effect of GABAergic therapy.

Treatment of dystonia is predominantly symptomatic. The therapeutic effect is rarely complete; more often, only a relative regression of dystonic manifestations is achieved. But this is also achieved at the cost of lengthy efforts to select drugs and their optimal doses. In addition, approximately 10% of dystonias are characterized by spontaneous remissions, in the presence of which it is difficult to talk about assessing the effectiveness of certain medications.

Traditionally, dopamine agonists and antagonists, anticholinergics, GABAergic and other drugs are used. Dopamine agonists (nacom, madopar, lisuride, midantan) and antagonists (haloperidol, pimozide, etopyrazine, azaleptin, tiapride, etc.) are effective in an equally low percentage of cases. Anticholinergics provide relief to almost every second patient. The most commonly used are cyclodol, parkopan, artane (trihexyphenidyl), but a dose of 2 mg in 1 tablet is rarely effective. Recently, Parkopan 5 mg has appeared, but even here the effect is often achieved at subtoxic doses. The use of cyclodol in daily doses even above 100 mg has been described. But at the same time, side effects are very likely, especially pronounced in patients of older age groups.

Among anticholinergics, Tremblex, a long-acting central anticholinergic, is more effective. Relief of dystonic manifestations is sometimes achieved approximately 50 - 80 minutes after one injection (2 ml) of the drug. Side effects - dry mouth, numbness and a feeling of furring of the tongue and throat, dizziness, feeling of intoxication, hypersomnia. This often forces the patient to refuse treatment with Tremblex. There is also a drop in the effectiveness of the drug, sometimes literally from injection to injection. Glaucoma is also a contraindication, especially in the treatment of older people.

In the treatment of dystonia, lithium salts (lithium carbonate) and clonidine (hemitone, clonidine) are used. Only a small proportion of patients respond well to treatment, but they need to be identified.

The vast majority of patients tolerate benzodiazepines well, especially clonazepam (antelepsin). But, unfortunately, we do not yet have an ampoule form of the drug. Clonazepam is effective for all types of diseases with the exception of generalized idiopathic torsion dystonia, where the effect is only subjective and can be explained by the psychotropic effect of the drug. Doses of clonazepam - from 3 to 6 - 8 mg per day, sometimes higher.

Blepharospasm, facial paraspasm (Bruegel's syndrome) and other cranial dystonias also respond well to clonazepam.

Among the drugs that have a relaxing effect in muscle spasticity, I would like to highlight the well-known, but until now undeservedly little used for muscular dystonia, mydocalm (tolperisone).

Muscular spasticity can be considered as a pathological state of balance, which quickly changes under the influence of various factors (fever, cold, heat, time of day, pain), so it is difficult to develop a medication that, thanks to a flexible dosage, would reduce the pathologically increased tone only to the desired level. And here tolperisone has, perhaps, the mildest effect, without crossing the “boundaries of what is permitted.”

Among the pharmacodynamic properties of tolperisone, the following should be highlighted: a central muscle relaxant effect and an independent increase in peripheral blood flow.

The localization of the muscle relaxant effect of the drug has been established in the following morphofunctional structures:

• in peripheral nerves;
• in the spinal cord;
• in the reticular formation.

Thanks to its membrane-stabilizing, local anesthetic effect, which manifests itself in the brain stem, spinal cord and peripheral nerves (both motor and sensory), mydocalm prevents the emergence and conduction of action potentials in “overstimulated” neurons and thereby reduces pathologically increased muscle tone. Depending on the dose, it inhibits nociceptive and non-nociceptive mono- and polysynaptic reflexes (flexion, direct and cross-extensor) in the spinal cord, inhibits mono- and polysynaptic reflexes at the level of the spinal roots, and also inhibits the conduction of excitation along the reticulospinal activating and blocking pathways.

Evidence of the direct effect of mydocalm on the brain stem is the blocking effect on tonic chewing reflexes that occur during periodontal stimulation. This reflex arc involves interneurons in the brainstem. A direct effect at the level of the brainstem is also evidenced by the effect of reducing the latent time of rotation-induced nystagmus.

Tolperisone significantly, dose-dependently, reduces rigidity caused by hyperactivity of gamma motor neurons after intercollicular transsection in the midbrain.

When ischemic rigidity occurs (in this case, the cause of rigidity is excitation arising in alpha motor neurons), tolperisone reduced its severity.

Large doses of tolperisone block the occurrence in experiments of seizures caused by provoking agents such as strychnine, electric shock, pentylenetetrazole.

The drug does not have a direct effect on the neuromuscular junction.

It is assumed that tolperisone has a weak atropine-like M-anticholinergic and slightly pronounced α-adrenergic blocking effects.

Pharmacological studies conducted on cats, rats, rabbits and dogs have shown that only with intravenous bolus administration of a high dose of tolperisone can a temporary sharp decrease in blood pressure occur. A longer, mild decrease in blood pressure is observed when using large doses of the drug (5 - 10 mg/kg).

In a study of dogs with bradycardia due to increased vagal tone, tolperisone slightly increased heart rate.

Tolperisone selectively and significantly increases blood flow in the femoral artery in dogs, while simultaneously decreasing mesenteric blood flow. Subsequently, when repeating the experiment using different methods on a large number of animals, it was revealed that this effect was due to a direct peripheral vasodilator effect.

After intravenous administration of tolperisone, lymph circulation increases.

The drug does not have a noticeable effect on the ECG.

All of the above turns out to be positive when mydocalm is prescribed to elderly and even geriatric patients suffering from various disorders of the cardiovascular system.

II. Myoclonic syndromes.

Myoclonus is a short jerky twitch of a muscle, similar to its contraction in response to a single electrical stimulation of the corresponding nerve. Myoclonus can be limited to a single (or individual) muscle, or involve many muscle groups up to complete generalization. Myoclonic jerks (jerks) can be synchronous or asynchronous, most of them are arrhythmic and may or may not be accompanied by movement in the joint. Their severity varies from a barely noticeable contraction to a sharp trembling, leading to a fall. Myoclonus tends to recur in the same muscles. There are spontaneous and reflex myoclonus, provoked by sensory stimuli of various modalities. There are myoclonus triggered by voluntary movement (actional and intentional myoclonus). Myoclonus is known to be dependent and independent of the sleep-wake cycle.

The pathophysiological and biochemical mechanisms of myoclonus are not well understood. Based on the location of generation of myoclonic discharges in the nervous system, 4 types of myoclonus are distinguished:

• cortical;
• stem (subcortical, reticular);
• spinal;
• peripheral.

The first two forms (cortical and stem) are of greatest clinical importance; they are more common than others. The presented classification is a modification of the old division of myoclonus into pyramidal, extrapyramidal and segmental forms.

The involvement of serotonergic mechanisms in the pathogenesis of myoclonus is assumed. Among patients, there are even subgroups that can be successfully treated with exactly the opposite means: some patients respond to agonists, others respond to serotonin antagonists.

Since a large number of diseases and nosological units can be accompanied by myoclonic hyperkinesis, several classifications of myoclonus have been proposed according to the etiological principle. Marsden's classification (1987) distinguishes 4 groups of myoclonus:

• physiological myoclonus;
• essential myoclonus;
• epileptic myoclonus;
• symptomatic myoclonus.

Examples of physiological myoclonus are myoclonus of falling asleep and waking up, myoclonus of fear, and some myoclonus in the form of hiccups. They usually do not require special treatment.

Essential myoclonus is familial as well as sporadic myoclonus, the so-called nocturnal myoclonus. They appear in the slow-wave sleep phase in patients with chronic insomnia. Can be treated with clonozepam, valproate, baclofen when using small doses (one tablet at night). Familial and sporadic myoclonus is a rare disorder called essential myoclonus or Friedreich's multiple paramyoclonus. The disease debuts in the first or second decade of life and is not accompanied by other neurological, mental and electroencephalographic disorders. Clinical manifestations include irregular, arrhythmic and asynchronous jerks and startles with a generalized distribution of myoclonus. Treatment is ineffective. Clonazepam and valproate are used.

Epileptic myoclonus is a myoclonus in the picture of an epileptic seizure, where it sometimes becomes one of the leading manifestations. There is a separate form of epilepsy - myoclonus epilepsy, considered even a hereditary disease that manifests itself in childhood.

Symptomatic myoclonus, most likely in the elderly and senile, is observed in a number of metabolic disorders, such as renal, hepatic or respiratory failure, alcohol intoxication, withdrawal of certain drugs, as well as in diseases that occur with structural damage to the brain (without epileptic seizures), such such as epidemic encephalitis, Creutzfeldt-Jakob disease, subacute sclerosing leukoencephalitis, postanoxic brain damage. The list of symptomatic myoclonus can be significantly expanded to include storage diseases (including Lafora body disease, sialidosis), paraneoplastic syndromes, toxic, including alcoholic, encephalopathies, with focal damage to the nervous system (angioma, ischemic or traumatic defect, stereotactic thalamotonia) , as well as myoclonus as a nonobligate side symptom of other diseases (lipidoses, leukodystrophies, tuberous sclerosis, spinocerebellar degenerations, Wilson-Konovalov disease, myoclonic dystonia, Alzheimer's disease, progressive supranuclear palsy, Whipple's disease). Progressive myoclonus epilepsy can, in principle, also be classified as symptomatic variants of myoclonus (based on epilepsy). The nosological independence of cerebellar myoclonic Ramsay-Hunt dyssynergia is also disputed. Only Ramsay-Hunt syndrome remains in use, which is equated as a synonym for myoclonus-epilepsy syndrome, Unferricht-Lundborg disease (“Baltic myoclonus”, progressive myoclonus-epilepsy). It seems necessary to us to dwell on the description of this pathology presented in the work of Italian authors C.A. Tassinari et al. (1994).

Unferricht-Lundborg disease is a form of progressive myoclonus epilepsy. This disease was better known in Finland traditionally under the name “Baltic myoclonus”. In recent years, an identical disease has been described in populations of Southern Europe - “Mediterranean myoclonus”, or “Ramsay Hunt syndrome”. In both populations, the disease has the same clinical and neurophysiological features: onset at 6–18 years of age, the appearance of active myoclonus, rare generalized seizures, mild symptoms of cerebellar insufficiency, absence of severe dementia, slow progression; The EEG reveals normal bioelectrical activity and generalized fast wave activity of the “peak” and “polypeak” type. The molecular genetic study showed the genetic unity of the disease in both populations: the localization of the defective gene on chromosome 22q22.3 was determined. However, in 3 out of 6 Italian families, the disease had atypical features - more rapid progression with dementia, the presence of occipital spikes on the EEG, which brings it closer to Lafora's disease. In this regard, it is possible that “Mediterranean myoclonus” is a heterogeneous syndrome.

Diagnostic criteria for Unferricht-Lunborg disease have been identified:

1. onset between 6 and 15, less often 18 years;
2. tonic-clonic seizures;
3. myoclonus;
4. EEG paroxysms in the form of spikes or polyspike-wave complexes with a frequency of 3 - 5 per second;
5. progressive course.

Some clinical forms of myoclonus:

Posthypoxic encephalopathy, in which the main manifestations are intentional and action myoclonus (Lance-Adams syndrome), sometimes in combination with dysarthria, tremor and ataxia.

Myoclonia of the soft palate (velo-palatine myoclonus - nystagmus of the soft palate, myorhythmia) - usually rhythmic, 2 - 3 per second, contractions of the soft palate, often in combination with hyperkinesis almost indistinguishable from tremor in the tongue, lower jaw, larynx, diaphragm and distal parts of the arms (classical myorhythmia, or “skeletal myoclonus”, as defined by old authors); myorhythmia disappears during sleep, can be either idiopathic or symptomatic (tumors in the pons and medulla oblongata, encephalomyelitis, trauma), sometimes ocular myoclonus of the “swinging” type is added. It is suppressed not only by clonazepam, like most myoclonus, but also by finlepsin (tegretol, stazepin, mazepine, carbamazepine).

Spinal (segmental) myoclonus: rhythmic, from 1 - 2 per minute to 10 per second; independent of external stimuli. The reasons lie in local damage to the spinal cord (myelitis, tumor, trauma, degeneration).

Opsoclonus (dancing eyes syndrome) is rapid, jerky, chaotic movements of the eyeballs. Increased hyperkinesis can sometimes occur explosively. Continues during sleep and even intensifies upon awakening. Opsoclonus is often mistaken for nystagmus, which is always distinguished by the presence of two sequential phases - slow and fast. Opsoclonus indicates organic damage to the cerebellar-stem connections in tumors of the brain stem and cerebellum, paraneoplastic syndromes, hemorrhages, severe trauma, metabolic and toxic encephalopathies in the final stage, multiple sclerosis and some other conditions. The “culprits” of opsoclonus are often viral encephalitis and meningoencephalitis. Children and people over 40 years of age are more likely to develop neuroblastoma. Treatment is carried out with adrenocorticotropic hormone, corticosteroids, obzidan, and benzodiazepine derivatives.

Myokymia of the superior oblique muscle of the eye (“unilateral rotatory nystagmus”); patients themselves feel characteristic molecular oscillopsia (“objects jumping up and down”, “eye swaying”, etc.) and torsion diplopia. The course is benign. There is a good therapeutic effect from finlepsin.

Hyperekplexia and the "Jumping Frenchman of Maine" syndrome. Hyperekplexia is pathologically increased involuntary shuddering, sometimes leading to the patient falling, occurring in response to unexpected tactile, light or sound stimuli. Sometimes it is an independent hereditary disease, and sometimes it is secondary, like the syndrome in Little, Creutzfeldt-Jakob diseases, and vascular lesions of the brain. With the “jumping Frenchman from Maine” syndrome, the frequency of paroxysms of bouncing reaches 100–120 times a day. Many are accompanied by falls and bruises, but without loss of consciousness. Helps clonozepam.

Hiccups are myoclonic contractions of the diaphragm and respiratory muscles. It can be physiological (after a heavy meal), a symptom of diseases of the gastrointestinal tract, chest organs, irritation of the phrenic nerve, damage to the brain stem or upper cervical segments of the spinal cord. Hiccups can be both toxicogenic and psychogenic. Treatment is carried out with neuroleptics, antiemetics (cerucal, for example), clonazepam, finlepsin, psycho- and physiotherapy, even transection of the phrenic nerve.

III. Other hyperkinetic syndromes.

The described syndromes include, first of all, perhaps, episodes of tremors and muscle cramps. In terms of the clarity and “picture” of their clinical manifestations, both tremor and some convulsions to some extent occupy an intermediate place between muscular dystonia and myoclonus, often including elements of both.

Muscle cramps refer to involuntary and painful contractions that occur spontaneously or after exercise. A necessary condition for the development of muscle cramps is the absence of regulatory opposition from antagonist muscles. When antagonistic muscles are tense, reciprocal blocking of convulsions occurs, but such blocking is also possible when skin efferent endings are involved.

Histologically, painfully contracting muscles reveal a large number of muscle fibers depleted of glycogen and isolated myolysis; this shows that cramps do not go away without leaving a trace, but have an effect on the structure of the muscles. Findings of this kind are partially comparable with the “syndrome of prolonged activity of muscle fibers” described by N. Isaacs and with other, less common syndromes, including those that develop with repeated irritation of peripheral nerves.

Often, muscle cramps and fascicular twitching are the first symptoms of general somatic disorders: abnormalities in electrolyte metabolism and metabolic disorders, including endocrine diseases, chronic inflammatory processes, and malignant tumors. Other reasons may be drug abuse (for example, nicotine and caffeine), various types of toxicosis, including medication. Hereditary nocturnal muscle cramps have also been described.

Diseases of the peripheral nerves and central nervous system can lead to muscle cramps. Convulsions can also occur when water-electrolyte metabolism is disrupted. Compression of muscle fibers due to swelling plays a significant role in the origin of cramping pain. The pain immediately disappears when the muscle fascia is cut. A similar mechanism may occur with ischemic cramps of the calf muscles, a predominantly sedentary lifestyle of most people, in which practically no muscle is involved. In peoples for whom squatting is common, when the muscles experience a relatively large load, cramps in the legs and other muscles are rare.

Some medications can induce muscle cramps or increase seizure activity. Any attempt to isolate certain groups of drugs, especially those affecting metabolism in muscles, affecting electrolytes or the functions of sarcolemmas and thereby predisposing to the development of muscle cramps, was practically unsuccessful, since the effect of medications is usually very multifaceted.

Muscle cramps are characteristic of tetanus. But it must be remembered that in this case muscle cramps are often complicated by changes in the tendons, including calcification (the shoulder, elbow and hip joints are most susceptible to this).
Among the endocrine diseases that can occur with characteristic muscle cramps, mention should be made of hypothyroidism.

Increased excitability and rigidity of all muscles of the neck, upper limbs and face in the patient were described by H. Mertens and K. Ricker as “spindle myotonia”. The picture of the disease is in many ways similar to the stiff-man syndrome that occurs sporadically in adults, described by F. Moersch and H. Woltman.

Schwartz-Jampel syndrome, or myotonic chondrodystrophy, which belongs to pseudomyotonia, is very interesting. Electromyography (EMG) in this disorder reveals characteristic explosive, irregularly repeating discharges similar to high-frequency discharges.

With neuromyotonia, persistent muscle contractions may spontaneously develop, covering the trunk and face. In this state, only slow active movements are possible. With both passive and active movements, muscle stiffness first increases and then decreases. The EMG shows irregular bursts of activity, after-discharges, and increased insertional activity (developing in response to the introduction of an electromyographic needle).

Myotonic syndromes, characterized by prolonged muscle contractions, can occur in response to their mechanical, electrical or other sufficiently strong activation.

Here are some of the most commonly developing muscle cramp syndromes.

Cramps: these are painful muscle spasms, primarily the muscles of the lower leg, as well as the abdomen, chest, back, and less commonly, the arms and face. More often we are talking about the triceps surae muscle. Occurs after physical activity, occurs in various diseases, including an autosomal dominant variant of non-progressive common cramps with minimal anterior horn deficiency; observed in amyotrophic lateral sclerosis, peripheral neuropathies, pregnancy, dysmetabolism. Quite often, crampy occurs in patients with lumbar osteochondrosis and in this case has the following features:

1. characteristic of the remission stage and almost never occurs in the acute period;
2. not being epileptic in nature, this local convulsive phenomenon is still often found in individuals with residual mild cerebral insufficiency;
3. it is characterized by local pathology, most often in the form of phenomena of popliteal neuroosteofibrosis;
4. it is caused by neurogenic mechanisms and humoral shifts - hyperacetylcholinemia, hyperserotoninemia (Popelyansky Ya.Yu.).

Like hypercalcemic, thyrotoxic and others, cramps with osteochondrosis are more common in older people and occur at night, in warmth, in a state of rest, i.e. under conditions that promote rapid and intense muscle shortening. Sudden shortening of the muscle is accompanied by an increase in its diameter, thickening (the muscle becomes sharply defined) and severe pain. Possible explanations for such pain lie partly in the biochemical plane (release of corresponding substances), partly in the electrophysiological plane (sudden loss of gate control, local discharge, formation of a pathological excitation generator). Clonazepam is effective.

Tics, facial hemispasm, restless legs syndrome (Ekbem), iatrogenic dyskinesias. Ticous generalized hyperkinesis is often combined with obsessive-compulsive disorders, which basically determines the clinical picture of Tourette syndrome, which accompanies various organic brain lesions. This syndrome must be differentiated from an independent nosology - Tourette's disease, which is hereditary. There are several points of view on the biochemical basis of Tourette's syndrome. Pfeifer C.C. et al. (1969) wrote about the deficiency of the enzyme hypoxanthine-guanine-phosphoribosyl-transferase, which is involved in the metabolic cycle of uric acid formation and is found in maximum concentration in the basal ganglia. P.V. Melnichuk et al. (1980) associate the syndrome in question with disorders of catecholamine metabolism. But one way or another, today in the treatment of tic hyperkinesis, the drug of choice is primarily haloperidol in a dose of 0.25 - 2.5 mg, prescribed before bedtime, and sometimes additionally during the daytime. Efficiency reaches 75 - 80% even with Tourette's syndrome or disease (Karlov V.A., 1996). The second-line drug is pimozide 0.5 - 10 mg per day. In elderly patients, the drug should be prescribed with caution and under ECG monitoring, as a prolongation of the P-Q interval has been noted. Clonazepam and reserpine are effective, but these drugs are still not as “successful” as antipsychotics.

Obsessive-compulsive disorders are well treated with antidepressants that inhibit serotonin reuptake. Monoamine oxidase inhibitors and tricyclic antidepressants (amitriptyline, imipramine) can be used. Psychostimulants may also be indicated: Meridil, Sidnocarb, but they enhance tic hyperkinesis. In recent years, the antidepressant fluoxetine (serotonin inhibitor) at a dose of 20 - 40 mg per day, deprenyl at a dose of 5 - 15 mg per day have been successfully used (Karlov V.A., 1996).

Tremor. With its non-parkinsonian origin (essential, alcoholic, thyrotoxic, post-traumatic tremor), we are talking about tremulous hyperkinesis that manifests itself during movement. If parkinsonian tremor is associated with dopaminergic deficiency, then non-parkinsonian tremor variants are based on the principle of excessive functioning of adrenergic and, possibly, GABAergic neurons. It is possible that there is also a violation of the stability of cell membranes, since anaprilin, which has the maximum effect on tremor, has a pronounced membrane-static effect (Elison P.H., 1978; Karlov V.A., 1996). Anaprilin (propranolol) sometimes causes severe allergic manifestations, even bronchospasm, and is therefore contraindicated for patients suffering from bronchial asthma or other allergies. In this case, the drug can be replaced with metoprol, oxprenolol (Trazicor), atenolol. Doses of beta-blockers for anaprilin are 60 - 80 mg per day. For elderly and senile people, small dosages are advisable, since side effects such as depression, sleep disorders, even toxic psychoses and hallucinosis occur more easily than in young people. In many patients, hexamidine (primiden) and clonazepam are effective. Leponex and isoniazid are used.

IV.Headaches.

Headache is one of the most common complaints with which patients consult a doctor of any specialty. According to statistical studies by various authors, the frequency of headaches ranges from 50 to 200 per 1000 population. Headache is the leading syndrome or symptom in more than 45 different diseases (Shtok V.N., 1987). The problem of headaches is so urgent that various specialized centers have been created to study it. The European Association for Headache Research was organized, and since 1991 the Russian Association has been a member of it. The work of the Association is coordinated by the Russian Headache Center, created on the basis of the Moscow Medical Academy named after. THEM. Sechenov.

Attempts have been made repeatedly to classify headaches. In our country, the pathogenetic classification of headaches presented by V.N. has become widely known. Stock and his famous monograph (1987). The author identifies 6 main types of headaches:

1. vascular;
2. muscle tension;
3. liquorodynamic;
4. neuralgic;
5. mixed;
6. psychalgia (central).

Each option has its own characteristic pathophysiological mechanism of headache. The author of this classification defends the concept of isolation of one of the indicated headache variants in each patient, while the mixed variant is considered a rare exception to the rule. As practice shows, this kind of approach is not always correct (Myakotnykh V.S., 1994), especially in patients with a polyetiological, polypathogenetic nature of the pathological process, one of the clinical manifestations of which is headache.

In elderly and senile people, in the process of accumulation of various diseases in them, headaches undoubtedly have a mixed, combined character, including various pathophysiological mechanisms of occurrence.

In 1988, the International Classification Committee proposed the most complete classification of headaches, which, however, is not final and continues to be improved, supplemented, and clarified. The classification considers the following forms of headaches:

• migraine:
  1. without aura (simple form);
  2. with aura (associated).

  In the latter, various forms are distinguished depending on the local symptoms that arise when the pathological focus is localized in a particular vascular basin;

• tension headaches (synonyms: psychalgia, psychomyogenic, neurotic); are divided into episodic and chronic, with or without involvement of the muscles of the scalp and (or) neck in the pathological process;
• cluster or cluster headaches;
• chronic paroxysmal hemicrania;
• headaches caused by vascular;
• infectious;
• tumor processes;
• traumatic brain injury, etc.

A very interesting and to a certain extent unusual, uncharacteristic for most other types of pathology is the fact that some types of headaches, in particular migraine, can be considered as a syndrome or even a symptom of any disease (even the terms “migraine” or “ migraine-like" syndrome), and as an independent nosological unit. Perhaps this has contributed to the fact that to this day there is no consensus on the frequency of occurrence of migraine, since some people understand this concept only as an independent disease, while others consider it a variant of a syndrome or even a symptom.

In addition, an absolutely reliable diagnosis of a particular type of headache is a difficult task. Based on the classification of 1988 and subsequent ones, it may seem that the simplest thing is to diagnose headaches “tied” to any specific pathology - vascular, infectious, tumor, traumatic, etc. To a certain extent, this is true, but only after the diagnosis of the “background” disease for the headache has already been made. Therefore, probably, the very factor of the presence of a headache in a patient from the very beginning should set the doctor up to diagnose the pathology in which headache acts as a symptom or syndrome. This kind of “cuts off” the last part of the classification, and the first part remains, where the diagnosis of the nature and clinical-pathogenetic, clinical-pathophysiological variant of the headache is carried out.

The most interesting in both clinical and pathophysiological aspects are probably the first three types of headache: migraine (occurs in the population with a frequency of 3 to 30% according to various authors); cluster or beam (frequency of occurrence from 0.05 to 6%); tension headaches (occur in 32 - 64%, and among other forms of headaches in women - up to 88%, in men - up to 69%). There are a number of common features that unite these three forms of headaches:

• All of them are psychogenic in nature;
• They are most represented in the population among other forms of headaches;
• The course is paroxysmal.

A sufficient severity of emotional and personal changes, although different in quality, is determined: migraine - a predominance of anxious, demonstrative traits, a high level of aspirations, low resistance to stress; tension headache - depressive-hypochondriacal, demonstrative character traits; cluster headache - “lion and mouse” syndrome (outwardly courageous, ambitious, ambitious, but internally timid and indecisive), with the presence of psychomotor agitation during the period of paroxysm.

The representation of clinical autonomic disorders is significant. The maximum vegetative disorders are presented in “panic migraine”, when at the height of the typical form of migraine signs of a panic attack appear (emotional arousal, fear, chill-like hyperkinesis, etc.).

There is a significant number of observations of muscular-tonic syndrome in the neck muscles (by palpation or according to the results of electroneuromyography). In migraine, this syndrome is predominantly expressed on the hemicrania side.

The proximity of subjective severity - the intensity of pain in paroxysm. According to the visual analogue scale (VAS): migraine - 78%, tension headache - 56%, cluster headache - 87%.

An important criterion is quality of life. It reflects the degree of adaptation of patients with these forms of headache, determines the degree of their activity, performance, feelings of fatigue, mood changes, and the effectiveness of the activities performed. Quality of life includes an assessment of the understanding and support of the patient by a loved one. The maximum decrease in quality of life in patients with tension headaches is up to 54%, for migraines - up to 70%, for cluster headaches (during an attack) - up to 86%.

Some similarity of disturbances in the interaction of noci- and antinociceptive systems in patients with migraine and tension-type headache at the level of the stem systems. This was revealed as a result of special biochemical and electrophysiological studies.

Thus, with the described forms of headaches, there is a certain psycho-vegetative-motor pattern that accompanies the pain paroxysm. This served as the basis for the use of not only widely known drugs described in numerous literature, but also psychotropic drugs and anticonvulsants for the treatment of headaches. For migraine, for example, phenobarbital, finlepsin, diphenin (Karlov V.A., 1987), kepra (Sherchever A.S. et al., 2007) are widely used. Anticonvulsants reduce the pain sensitivity of the vascular wall and enhance antinociception at the level of the stem systems. For cluster headaches, sodium valproate is used, which is a GABA mimetic and acts on the interneurons of the hypothalamus, thereby affecting circadian rhythms, the disruption of which is one of the main pathogenetic links in cluster cephalgia. Finlepsin can be used in combination with other analgesic, vascular drugs, and sedatives.

For migraines and tension headaches, tricyclic antidepressants are used, especially amitriptyline, due to the presence of psychovegetative and psychomotor clinical manifestations in paroxysms. The use of alprozolam (cassadana) has proven to be quite effective, especially for headaches of neurotic or partially neurotic origin. Since this drug has an anxiolytic, antidepressant, muscle relaxant effect, and affects the GABAergic system, it can be used for the following types of headaches: panic migraine, combined migraine plus tension headaches, predominantly episodic tension headaches with the presence of muscle dysfunction.

The question of interest is whether it is possible and how often it is possible to combine several types of headache in one patient and whether a change, or even “kaleidoscopicity” (a constant change of options with periodic repetitions) is possible in the same patient. At the same time, of course, two more questions often arise: what is this connected with and how to solve therapeutic problems?

From the indicated positions, two main options for a clinical “change of scenery” can be considered:

1. one patient simultaneously experiences several variants of one type of headache, for example, several variants of migraine attacks;
2. One patient has several types of headaches.

Perhaps the various variants of migraine are described most fully and clearly. Let us once again cite the main ones.

1. Simple form (no aura).
2. Associated form (with aura).

In the latter form, a number of clinical variants can be distinguished depending on the clinical picture of the aura (ophthalmic, ophthalmoplegic, olfactory, illusory, vestibular, etc.).

V. Autonomic disorders.

According to epidemiological studies, up to 80% of the population experiences some kind of vegetative disorders. This is due to the key role of the autonomic nervous system in such basic processes as maintaining homeostasis and adapting to changing environmental conditions. Events and situations of both a biological and psychosocial nature can lead to a breakdown of autonomic regulation, which clinically manifests itself in the form of autonomic dysfunction or autonomic dystonia syndrome. Completely incorrect, in our opinion, is the opinion that with age, vegetative-dystonic manifestations become less pronounced than in young people, and the total number of patients suffering from neurocirculatory or vegetative-vascular dystonia drops sharply. It seems to us, on the contrary, that the number of patients with dystonic, vegetative-vascular pathological manifestations in the elderly and senile age is increasing, but this pathology is moving from the category of nosology or syndromology to predominantly symptomatic aspects. Various clinical variants of atherosclerosis, arterial hypertension, pathological processes in the gastrointestinal tract, urinary, endocrine systems, osteochondrosis, and finally, come first as an independent disease or syndrome. All these diseases can be clinically represented by vegetative-dystonic disorders, but these disorders are no longer perceived as syndromes, not as independent diseases, but as one, two or more symptoms of more severe pathological processes. This does not mean at all that in old age the problem of vegetative-vascular dystonia is absent or at least fades into the background. After all, if we cannot completely stop the development of atherosclerosis, for example, then it would be wrong to completely abandon symptomatic treatment; the patient is not worried about the disease as such, he is worried about the manifestations of this disease. And therefore, in the elderly, very often therapy can and should be aimed specifically at manifestations that level the quality of life of our patients. Within the framework of vegetative dystonia syndrome, it is customary to distinguish 3 groups of autonomic disorders(Vein A.M., 1988):

• psycho-vegetative syndrome;
• progressive autonomic failure syndrome;
• vegetative-vascular-trophic syndrome.

In some cases, autonomic disorders are of a constitutional nature, manifesting themselves from early childhood or puberty, but in most patients they develop secondary, as part of neuroses, psychophysiological reactions, against the background of hormonal changes, organic somatic, neurological diseases, and endogenous mental disorders.

Particularly noteworthy is the group of psycho-autonomic disorders, which occur most often and clinically manifest themselves in the form of emotional disorders in combination with multisystem autonomic disorders (cardiovascular system, breathing, gastrointestinal tract, thermoregulation, sweating, etc.). These disorders can occur in the form of permanent, paroxysmal, permanent-paroxysmal disorders. The most obvious and striking representatives of autonomic disorders of this group are autonomic crises (panic attacks) and neurogenic fainting (syncope).

Panic attacks are the most dramatic manifestation of autonomic dystonia syndrome (Vein A.M. et al., 1994). Many terms have been proposed that denote apparently identical conditions: diencephalic crises, cerebral vegetative seizures, hyperventilation attacks, anxiety attacks, etc. It seems necessary to us, therefore, when considering panic attacks, to at least briefly dwell on the problem of vegetative-vascular dystonia

For many years, vegetative-vascular dystonia was considered either within the framework of neuroses, or as a pathology of the autonomic nervous system, or as the initial form of other diseases, for example, arterial hypertension, cerebral atherosclerosis. However, vegetative-vascular dystonia is an independent form of pathology, which essentially has etiopathogenetic relationships and is a functional disease of polyetiological origin, manifested mainly by vascular and vetetative disorders.

Let us consider the chain of pathophysiological and biochemical reactions that occur during vegetative-vascular dystonia. The most important, perhaps, is the question of the formation of functional hypoxia of the brain. Several mechanisms are important in its occurrence: hyperventilation as a manifestation of a sympathotonic effect followed by a vasoconstrictor effect of the microvasculature. There is a direct vasoconstrictor effect due to an increase in the levels of adrenaline, norepinephrine and cortisol (as a nonspecific effect of stress activation) with a subsequent decrease in maximum oxygen consumption, a decrease in metabolism and a slowdown in lactate utilization. Finally, there is a change in the rheological properties of blood (increased viscosity, aggregation properties of erythrocytes and platelets), hemoglobin tropism for oxygen, which, in combination with microcirculation disorders, aggravates the level of brain hypoxia. With emotional stress, the body's need for energy increases, which is compensated mainly by increasing lipid metabolism.

The processes of lipid peroxidation play an important role in the development of adaptation diseases associated with stress and, in particular, diseases of the cardiovascular system. Many authors in their works point to the activation of lipid peroxidation in gastric and duodenal ulcers, neurodermatitis and diabetes. In animal experiments, in response to severe stress, lipid peroxides accumulated, which led to damage to body tissues, and the introduction of antioxidants inhibited the development of stress-related disorders of internal organs with a sharp decrease in the release of corticosteroid hormones. Relationships between the activity of lipid peroxidation and the clinical features of neurotic disorders were revealed. It is obvious that microcirculation disorders and brain hypoxia are the intermediate link that transforms the psychogenic effect into a stable pathological state of the brain. This dictates the need to include in the therapeutic complex drugs used in the treatment of neuroses and, in particular, vegetative-vascular dystonia, which, in addition to affecting the listed biological targets (blood aggregation properties, microcirculation disorders, oxygen metabolism and lipid peroxidation processes of biological membranes), disrupted would be a chain of pathological adaptive reactions to anxiety and indirectly reduce the severity of emotional stress.

Since 1980, with the advent of the American Classification of Mental Illnesses (DSM - III), the term “panic attack” has been established in international practice to denote paroxysmal states with multisystem vegetative, emotional and cognitive disorders. These conditions are included in the broader class of “anxiety conditions.” The main criteria for identifying panic attacks are:

• recurrence of attacks;
• their occurrence outside of emergency and life-threatening situations;
• attacks are manifested by a combination of at least 4 of the 13 symptoms listed below:
• dyspnea;
• “pulsation”, tachycardia;
• pain or discomfort in the left side of the chest;
• feeling of suffocation;
• dizziness, unsteadiness, feeling of impending fainting;
• feeling of derealization, depersonalization;
• nausea or abdominal discomfort;
• chills;
• paresthesia in the arms and legs;
• sensation of “hot flashes”, “waves” of heat or cold;
• sweating;
• fear of death;
• fear of going crazy or committing an uncontrollable act.

Panic attacks occur in 1 - 3% of the population, twice as often in women and mainly between the ages of 20 and 45, although in menopause they are also not a rare occurrence. The clinical picture of suffering is represented by paroxysms, the core of which is the above symptoms. However, it was noted that in a number of patients at the time of the attack there is no feeling of fear or anxiety (“panic without panic”, “non-fearful attacks”), in some patients emotional manifestations may consist of a feeling of melancholy or depression, in others it is irritation, aggression or just internal tension. Most patients have functional neurotic symptoms during an attack: a lump in the throat, pseudoparesis, speech and voice disorders, convulsive phenomena, etc. Attacks can occur both spontaneously and situationally; in some patients they develop at night, during sleep, often accompanied by unpleasant, disturbing dreams. The latter often precede the onset of the attack at the moment of waking up, and after the end of the panic attack they become completely or partially amnesic. When paroxysms are repeated, a feeling of anxious anticipation is formed, and then so-called avoidant behavior. The latter, in its extreme form, acts as an agoraphobic syndrome (patients become completely maladapted, cannot stay at home alone, move unaccompanied on the street, city transport is excluded, etc.). In 30% of cases, the recurrence of panic attacks leads to the emergence and development of depressive syndrome. Hysterical and hypochondriacal disorders are common.

Syncope (neurogenic syncope). The general concept of syncope is as follows: “Fainting is a short-term disturbance of consciousness and postural tone due to reversible disturbances of brain function with spontaneous recovery.”

Fainting occurs in 3% of the population, but at puberty the frequency of repeated syncope can reach 30% (Vein A.M. et al., 1994). There is no single classification of fainting yet, but all researchers of this problem identify 2 main groups of fainting:

1. neurogenic (reflex),
2. somatogenic (symptomatic).

The first include:

• vasodepressor syncope;
• orthostatic syncope;
• sinocarotid;
• hyperventilation;
• tussive;
• nocturic;
• fainting when swallowing and with glossopharyngeal neuralgia.

Among the second group of fainting are:

• associated with cardiac pathology, where impaired cardiac output occurs due to cardiac arrhythmias or mechanical obstruction to blood flow;
• associated with hypoglycemia;
• associated with peripheral autonomic failure;
• associated with pathology of the carotid and vertebrobasilar arteries;
• associated with organic damage to the brain stem;
• hysterical pseudosyncope, etc.

The clinical picture of syncope is quite stereotypical. The syncopation itself usually lasts from a few seconds to 3 minutes; the patient turns pale, muscle tone decreases, mydriasis is noted with a decrease in the pupils' reactions to light, a weak, labile pulse, shallow breathing, and a decrease in blood pressure. With deep syncope, there may be several tonic or clonic-tonic jerks, involuntary urination and defecation.

There are pre- and post-syncope symptoms.

Presyncope (lipothymia), lasting from a few seconds to 2 minutes, is manifested by a feeling of lightheadedness, nausea, general discomfort, cold sweat, dizziness, blurred vision, muscle weakness, tinnitus and a feeling of passing consciousness. A number of patients experience fear, anxiety, palpitations, a feeling of lack of air, paresthesia, “lump in the throat,” i.e. symptoms of a panic attack. After an attack, patients quickly come to their senses, although they are alarmed, pale, have tachycardia, and general weakness.

Most patients clearly identify factors that provoke fainting: stuffiness, prolonged standing, getting up quickly, emotional and pain factors, transport, vestibular stress, overheating, hunger, alcohol, lack of sleep, premenstrual period, getting up at night, etc.

Some aspects of the pathogenesis of panic attacks and syncope may be very similar and at the same time have distinct differences. Psychological and biological aspects of pathogenesis are distinguished. From a psychophysiological point of view, syncope is a pathological reaction that occurs as a result of anxiety or fear in conditions where motor activity (fight or flight) is impossible. From the point of view of psychodynamic concepts, a panic attack is a signal to the ego about the threat of suppressed, unconscious impulses to mental balance. A panic attack helps the ego to prevent an unconscious aggressive or sexual impulse from "spurting out" which could lead to more serious consequences for the individual.

Currently, the biological factors in the pathogenesis of fainting and panic attacks are being actively studied. The physiological mechanisms for the implementation of these two states are to a certain extent opposite. In patients with syncope due to sympathetic failure (especially in the sympathetic postganglionic fibers of the lower extremities), active vasodilation occurs, which leads to a decrease in cardiac output. In panic attacks, on the contrary, vascular insufficiency is detected, which is supported by:

1. development of spontaneous panic attacks during the period of relaxation;
2. a sharp increase in heart rate over a short period of time;
3. decrease in the content of adrenaline, norepinephrine in the blood serum in the pre-crisis period;
4. characteristic changes in the oscillatory structure of the heart rhythm (detected by cardiointervalography, for example).

When studying the central mechanisms of the pathogenesis of mainly panic attacks, a direct relationship of the noradrenergic nucleus of the brain stem to anxious behavior was shown. It is no coincidence that drugs that affect noradrenergic systems—tricyclic antidepressants and monoamine oxidase inhibitors (MAOIs)—have become so widespread in the treatment of panic attacks. The role of serotonergic systems in the pathogenesis of panic attacks has been widely studied. The result is the creation of a large group of drugs whose action is aimed at these systems - clomipramine, zimeldine, fluvoxamine, fluvoxetine.

Of particular interest is the biochemical systems associated with the functions of excitation and inhibition - glutamatergic and GABAergic. These systems play a key and opposing role in the realization of both anxiety; as well as paroxysmalness. In this regard, it seems appropriate to summarize the main clinical and experimental data indicating the proximity of paroxysmal vegetative states and epilepsy:

There are a number of common provoking factors - hyperventilation, inhalation of carbon dioxide;

Paroxysmal course;

Both spontaneous panic attacks and epileptic seizures most often occur during periods of relaxed wakefulness, often during the stage of slow-wave sleep. 2/3 of patients with panic attacks react to sleep deprivation, including electroencephalographically, similarly to patients with epilepsy;

In patients with fainting, paroxysmal activity on the EEG and a decrease in the convulsive threshold are often recorded, as well as asymmetric involvement of the deep temporal formations, which is also typical for patients with epilepsy;

Relatives of patients suffering from panic attacks or fainting often experience typical epileptic seizures;

Autonomic crises can often be risk factors for the subsequent occurrence of epileptic paroxysms, especially in adults (Myakotnykh V.S., 1992);

The therapeutic activity of antiepileptic drugs (anticonvulsants) in patients with fainting and panic attacks is high.

Treatment of vegetative paroxysms.

Until the mid-1980s, antidepressants dominated the treatment of panic attacks. Basic drugs were considered tricyclic antidepressants (imipramine, amitriptyline, etc.), MAO inhibitors (phenelzine), and four-cyclic antidepressants (mianserin, pyrazidol). But the side effects turned out to be significant, problems arose with increasing the dose, the obvious first effect appeared only after 14 - 21 days, while on days 10 - 12 an exacerbation of the disease was observed - anxiety increased, attacks became more frequent. Patients also experienced increased blood pressure (BP) and persistent tachycardia, decreased potency, and weight gain.

Now the emphasis in drug treatment has shifted to a group of drugs that act primarily on GABAergic systems. Benzodiazepines are exogenous ligands of benzodiazepine receptors, the mediator of which is GABA. There are at least 2 types of central benzodiazepine receptors (BRR): BDR-1, responsible for anti-anxiety and anticonvulsant effects, and BDR-2, responsible for the sedative (hypnotic) effect and muscle relaxant effect. The effects of a new generation of drugs (atypical benzodiazepines), the most famous of which are clonazepam (Antelepsin) and alprozolam (Xanax, Cassadane), are associated with a specific effect on BDR-1.

Clonazepam gives a clear anti-panic effect at a dose of 2 mg per day with 1-2 doses. The effect of treatment occurs already in the first week. The effectiveness of the drug is up to 84% (Vein A.M. et al., 1994). Side effects are minimal. The independence of the effect from the duration of the disease and effectiveness in persons with previous attacks of alcoholic excesses, who even complain of a hereditary burden of alcoholism, are specific. To a lesser extent, clonazepam affects the secondary symptoms of panic attacks - depression and agoraphobia, which makes it advisable to include antidepressants in therapy. At a dose of 3 - 4 mg per day, the drug has proven itself in the treatment of syncopal paroxysms, lipothymia and “hot flashes” during menopause.

Alprozolam is 85 to 92% effective against panic attacks. The effect is in the first week of treatment. The drug relieves anxiety and normalizes social and family maladjustment. There is also a fairly pronounced antidepressant effect, but for agoraphobia it is still advisable to add antidepressants to the treatment. The drug can be used for long courses of treatment (up to 6 months) and for maintenance therapy, and does not require increasing doses. The range of doses used is from 1.5 to 10 mg per day, on average 4 - 6 mg. It is recommended to take it in fractional doses. Main side effects: sedation, drowsiness, fatigue, memory loss, libido, weight gain, ataxia. The drug should not be prescribed to patients with substance abuse and alcoholism, because it is possible to develop dependence on the drug. A gradual reduction in dosage at the end of the course of treatment is recommended.

Finlepsin has been increasingly used in recent years in the treatment of paroxysmal conditions of non-epileptic origin.

I would especially like to mention such a well-known drug as Cavinton (vinpocetine), Cavinton-Forte. Cavinton, as a drug that optimizes metabolism (neurometabolic cerebroprotector) and hemodynamics of the brain, can be considered as a means of influencing the pathogenetic mechanisms of the formation of vegetative-vascular dysfunctions. In addition, a number of works indicate the use of Cavinton to target anxiety, which is a concomitant symptom of various neurotic manifestations. In addition, Cavinton has a pronounced vegetotropic effect, which consists in reducing the reactivity of the sympathetic department of the autonomic nervous system. All this makes it possible to successfully use this drug in the treatment of neuroses and autonomic dysfunctions.

In the treatment of non-epileptic paroxysmal conditions, physiotherapy and balneotherapy, psychotherapy, acupuncture, and bioenergetic effects are widely used. Methods and duration of exposure are selected strictly individually and do not contradict the prescription of basic drug therapy.